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  • 1.
    Abrahamsson, Thomas
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn- och ungdomskliniken i Linköping.
    Sherman, Philip M.
    University of Toronto, Canada .
    Editorial Material: Multifaceted Effects of Human Milk Oligosaccharides2014Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 209, nr 3, s. 323-324Artikel i tidskrift (Övrigt vetenskapligt)
    Abstract [en]

    n/a

  • 2. Anantharajah, Ahalieyah
    et al.
    Faure, Emmanuel
    Buyck, Julien M.
    Sundin, Charlotta
    Creative Antibiotics, Umeå, Sweden .
    Lindmark, Tuulikki
    Mecsas, Joan
    Yahr, Timothy L.
    Tulkens, Paul M.
    Mingeot-Leclercq, Marie-Paule
    Guery, Benoît
    Van Bambeke, Françoise
    Inhibition of the Injectisome and Flagellar Type III Secretion Systems by INP1855 Impairs Pseudomonas aeruginosa Pathogenicity and Inflammasome Activation2016Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 214, nr 7, s. 1105-1116Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    With the rise of multidrug resistance, Pseudomonas aeruginosa infections require alternative therapeutics. The injectisome (iT3SS) and flagellar (fT3SS) type III secretion systems are 2 virulence factors associated with poor clinical outcomes. iT3SS translocates toxins, rod, needle, or regulator proteins, and flagellin into the host cell cytoplasm and causes cytotoxicity and NLRC4-dependent inflammasome activation, which induces interleukin 1 beta (IL-1 beta) release and reduces interleukin 17 (IL-17) production and bacterial clearance. fT3SS ensures bacterial motility, attachment to the host cells, and triggers inflammation. INP1855 is an iT3SS inhibitor identified by in vitro screening, using Yersinia pseudotuberculosis. Using a mouse model of P. aeruginosa pulmonary infection, we show that INP1855 improves survival after infection with an iT3SS-positive strain, reduces bacterial pathogenicity and dissemination and IL-1 beta secretion, and increases IL-17 secretion. INP1855 also modified the cytokine balance in mice infected with an iT3SS-negative, fT3SS-positive strain. In vitro, INP1855 impaired iT3SS and fT3SS functionality, as evidenced by a reduction in secretory activity and flagellar motility and an increase in adenosine triphosphate levels. As a result, INP1855 decreased cytotoxicity mediated by toxins and by inflammasome activation induced by both laboratory strains and clinical isolates. We conclude that INP1855 acts by dual inhibition of iT3SS and fT3SS and represents a promising therapeutic approach.

  • 3.
    Benson, Mikael
    et al.
    East Hospital, Göteborg, Sweden.
    Jodal, Ulf
    Göteborg University, Sweden.
    Agace, William
    Lund University, Sweden.
    Hellström, Mikael
    Sahlgrenska University Hospital, Göteborg, Sweden.
    Mårild, Staffan
    Sahlgrenska University Hospital, Göteborg, Sweden.
    Rosberg, Sten
    Göteborg University, Sweden.
    Sjöström, Michael
    Umeå University, Sweden.
    Wettergren, Björn
    Jönsson, Susanne
    Svanborg, Catharina
    Lund University, Sweden.
    Interleukin (IL)-6 and IL-8 in children with febrile urinary tract infection and asymptomatic bacteriuria1996Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 174, nr 5, s. 1080-1084Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Urine and serum interleukin (IL)-6 and IL-8 responses were higher in children with febrile urinary tract infection (n = 61) than in those with asymptomatic bacteriuria (n = 39). By univariate analysis, cytokine levels were related to age, sex, reflux, renal scarring, urine leukocytes, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and bacterial properties (P fimbriae but not hemolysin). Multivariate modeling showed that urine IL-6 responses were higher in girls than boys, increased with age, and were positively associated with CRP, ESR, serum IL-6, and urine leukocyte counts. The urine IL-8 response was not influenced by age, but it was influenced by P fimbriae and was associated with ESR, CRP, urine leukocytes, and female sex. The results show that cytokine responses to urinary tract infection vary with the severity of infection and that cytokine activation is influenced by a variety of host and bacterial variables.

  • 4.
    Berg, Aase
    et al.
    Stavanger University Hospital, Norway ; University of Bergen, Norway.
    Otterdal, Kari
    Oslo University Hospital Rikshospitalet, Norway.
    Patel, Sam
    Central Hospital of Maputo, Mozambique.
    Gonca, Miguel
    Central Hospital of Maputo, Mozambique.
    David, Catarina
    Central Hospital of Maputo, Mozambique.
    Dalen, Ingvild
    Stavanger University Hospital, Norway.
    Nymo, Stig
    Oslo University Hospital Rikshospitalet, Norway.
    Nilsson, Margareta
    Oslo University Hospital Rikshospitalet, Norway.
    Nordling, Sofia
    Uppsala University.
    Magnusson, Peetra U
    Uppsala University.
    Ueland, Thor
    Oslo University Hospital Rikshospitalet, Norway.
    Prato, Mauro
    University of Torino, Italy.
    Giribaldi, Giuliana
    University of Torino, Italy.
    Mollnes, Tom Eirik
    Oslo University Hospital Rikshospitalet, Norway.
    Aukrust, Pål
    Oslo University Hospital Rikshospitalet, Norway.
    Langeland, Nina
    University of Bergen, Norway.
    Nilsson, Per H.
    Oslo University Hospital Rikshospitalet, Norway.
    Complement Activation Correlates With Disease Severity and Contributes to Cytokine Responses in Plasmodium falciparum Malaria.2015Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 212, nr 11, s. 1835-1840Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The impact of complement activation and its possible relation to cytokine responses during malaria pathology was investigated in plasma samples from patients with confirmed Plasmodium falciparum malaria and in human whole-blood specimens stimulated with malaria-relevant agents ex vivo. Complement was significantly activated in the malaria cohort, compared with healthy controls, and was positively correlated with disease severity and with certain cytokines, in particular interleukin 8 (IL-8)/CXCL8. This was confirmed in ex vivo-stimulated blood specimens, in which complement inhibition significantly reduced IL-8/CXCL8 release. P. falciparum malaria is associated with systemic complement activation and complement-dependent release of inflammatory cytokines, of which IL-8/CXCL8 is particularly prominent.

  • 5. Birse, Kenzie D.
    et al.
    Romas, Laura M.
    Guthrie, Brandon L.
    Nilsson, Peter
    KTH, Skolan för bioteknologi (BIO), Proteomik och nanobioteknologi. KTH, Centra, Science for Life Laboratory, SciLifeLab.
    Bosire, Rose
    Kiarie, James
    Farquhar, Carey
    Broliden, Kristina
    Burgener, Adam D.
    Genital Injury Signatures and Microbiome Alterations Associated With Depot Medroxyprogesterone Acetate Usage and Intravaginal Drying Practices2017Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 215, nr 4, s. 590-598Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background. Increasing evidence suggests depot medroxyprogesterone acetate (DMPA) and intravaginal practices may be associated with human immunodeficiency virus (HIV-1) infection risk; however, the mechanisms are not fully understood. This study evaluated the effect of DMPA and intravaginal practices on the genital proteome and microbiome to gain mechanistic insights. Methods. Cervicovaginal secretions from 86 Kenyan women, including self-reported DMPA users (n = 23), nonhormonal contraceptive users (n = 63), and women who practice vaginal drying (n = 46), were analyzed using tandem-mass spectrometry. Results. We identified 473 human and 486 bacterial proteins from 18 different genera. Depot medroxyprogesterone acetate use associated with increased hemoglobin and immune activation (HBD, HBB, IL36G), and decreased epithelial repair proteins (TFF3, F11R). Vaginal drying associated with increased hemoglobin and decreased phagocytosis factors (AZU1, MYH9, PLAUR). Injury signatures were exacerbated in DMPA users who also practiced vaginal drying. More diverse (H index: 0.71 vs 0.45; P =.009) bacterial communities containing Gardnerella vaginalis associated with vaginal drying, whereas DMPA showed no significant association with community composition or diversity. Conclusions. These findings provide new insights into the impact of DMPA and vaginal drying on mucosal barriers. Future investigations are needed to confirm their relationship with HIV risk in women.

  • 6. Boman, J
    et al.
    Söderberg, Stefan
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Kardiologi.
    Forsberg, J
    Birgander, L S
    Allard, A
    Persson, K
    Jidell, E
    Kumlin, U
    Juto, P
    Waldenström, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Kardiologi.
    Wadell, G
    High prevalence of Chlamydia pneumoniae DNA in peripheral blood mononuclear cells in patients with cardiovascular disease and in middle-aged blood donors.1998Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 178, nr 1Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Nested polymerase chain reaction (nPCR) demonstrated the presence of Chlamydia pneumoniae-specific DNA in peripheral blood mononuclear cells (PBMC). PBMC samples were obtained from 103 consecutive patients (62 male, 41 female) aged 22-85 years (mean, 64) admitted for coronary angiography because of suspected coronary heart disease and from 52 blood donors (43 male, 9 female) aged 40-64 years (mean, 49). Of the 101 evaluable patients, 60 (59%) were identified by nPCR assay as C. pneumoniae DNA carriers; C. pneumoniae-specific microimmunofluorescence (MIF) serology confirmed exposure to the bacterium in 57 (95%) of the 60 nPCR-positive patients. Among the 52 blood donors, the nPCR assay identified 24 (46%) C. pneumoniae DNA carriers, all of whom were positive by C. pneumoniae-specific serology. Thirty-two patients (32%) and 23 blood donors (44%) were MIF antibody-positive but repeatedly nPCR-negative; Bartonella henselae- or Bartonella quintana-specific antibodies were not detected among any of these subjects. In this study, C. pneumoniae DNA was common in PBMC of patients with coronary heart disease and in middle-aged blood donors.

  • 7. Browall, Sarah
    et al.
    Norman, Martin
    Tångrot, Jeanette
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten). Bioinformatics Infrastructure for Life Sciences, Computational Life Science Cluster.
    Galanis, Ilias
    Sjöstrom, Karin
    Dagerhamn, Jessica
    Hellberg, Christel
    Pathak, Anuj
    Spadafina, Tiziana
    Sandgren, Andreas
    Bättig, Patrick
    Franzén, Oscar
    Andersson, Björn
    Örtqvist, Åke
    Normark, Staffan
    Henriques-Normark, Birgitta
    Intraclonal Variations Among Streptococcus pneumoniae Isolates Influence the Likelihood of Invasive Disease in Children2014Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 209, nr 3, s. 377-388Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background. Pneumococcal serotypes are represented by a varying number of clonal lineages with different genetic contents, potentially affecting invasiveness. However, genetic variation within the same genetic lineage may be larger than anticipated. Methods. A total of 715 invasive and carriage isolates from children in the same region and during the same period were compared using pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing. Bacterial genome sequencing, functional assays, and in vivo virulence mice studies were performed. Results. Clonal types of the same serotype but also intraclonal variants within clonal complexes (CCs) showed differences in invasive-disease potential. CC138, a common CC, was divided into several PFGE patterns, partly explained by number, location, and type of temperate bacteriophages. Whole-genome sequencing of 4 CC138 isolates representing PFGE clones with different invasive-disease potentials revealed intraclonal sequence variations of the virulence-associated proteins pneumococcal surface protein A (PspA) and pneumococcal choline-binding protein C (PspC). A carrier isolate lacking PcpA exhibited decreased virulence in mice, and there was a differential binding of human factor H, depending on invasiveness. Conclusions. Pneumococcal clonal types but also intraclonal variants exhibited different invasive-disease potentials in children. Intraclonal variants, reflecting different prophage contents, showed differences in major surface antigens. This suggests ongoing immune selection, such as that due to PspC-mediated complement resistance through varied human factor H binding, that may affect invasiveness in children.

  • 8.
    Bröms, Jeanette
    et al.
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet). Department of Medical Countermeasures, Swedish Defence Research Agency.
    Forslund, Anna-Lena
    Department of Medical Countermeasures, Swedish Defence Research Agency.
    Forsberg, Åke
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet). Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten). Department of Medical Countermeasures, Swedish Defence Research Agency.
    Francis, Matthew
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten). Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    PcrH of Pseudomonas aeruginosa is essential for secretion and assembly of the type III translocon2003Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 188, nr 12, s. 1909-1921Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Pseudomonas aeruginosa harbors a type III secretion system that translocates antihost effectors into an infected eukaryotic cell. PcrH is a key component of type III secretion in this essential virulence strategy. In the absence of PcrH, P. aeruginosa is translocation deficient because of a specific reduction in presecretory stability and subsequent secretion of PopB and PopD, 2 proteins essential for the translocation process. PcrH exerts this chaperone function by binding directly to PopB and PopD. Consistent with the genetic relatedness of PcrH with LcrH of pathogenic Yersinia species, these proteins are functionally interchangeable with respect to their ability to complement the translocation defect associated with either a lcrH or pcrH null mutant, respectively. Thus, the translocator class of chaperones performs a critical function in ensuring the assembly of a translocation competent type III secreton. Finally, unlike the regulatory roles of other translocator-class chaperones (e.g., LcrH, SicA of Salmonella enterica, and IpgC of Shigella species), in vitro regulation of P. aeruginosa type III secretion does not involve PcrH.

  • 9.
    Bröms, Jeanette
    et al.
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Sundin, Charlotta
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Francis, Matthew
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet). Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
    Forsberg, Åke
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten). Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Comparative analysis of type III effector translocation by Yersinia pseudotuberculosis expressing native LcrV or PcrV from Pseudomonas aeruginosa2003Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 188, nr 2, s. 239-249Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The homologues LcrV of Yersinia species and PcrV of Pseudomonas aeruginosa are pore-forming components. When expressed in a Yersinia lcrV background, PcrV formed smaller pores in infected erythrocyte membranes, correlating to a lowered translocation of Yersinia effectors. To understand this phenomenon, cytotoxins exoenzyme S of P. aeruginosa and YopE of Yersinia were introduced into a Yersinia background without Yop effectors but expressing LcrV or PcrV. Comparable translocation of each substrate indicated that substrate recognition by LcrV/PcrV is not a regulator of translocation. Yersinia harboring pcrV coexpressed with its native operon efficiently translocated effectors into HeLa cell monolayers and formed large LcrV-like pores in erythrocyte membranes. Thus, a PcrV complex with native P. aeruginosa translocon components is required to form fully functional pores for complete complementation of effector translocation in Yersinia.

  • 10.
    Cardell, Kristina
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Infektionsmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Infektionskliniken i Östergötland.
    Åkerlind, Britt
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Klinisk mikrobiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk mikrobiologi.
    Sällberg, Matti
    Division of Clinical Virology, Karolinska Institute at Karolinska University Hospital, Huddinge, Sweden.
    Frydén, Aril
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Infektionsmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Närsjukvården i centrala Östergötland, Infektionskliniken US.
    Excellent response rate to a double dose of the combined hepatitis A and B vaccine in previous nonresponders to hepatitis B vaccine2008Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 198, nr 3, s. 299-304Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Hepatitis B vaccine has been shown to be highly efficient in preventing hepatitis B. However, 5%-10% of individuals fail to develop protective levels (>or=10 mIU/mL) of antibodies to hepatitis B surface antigen (anti-HBs) and are considered to be nonresponders.

    METHODS: A total of 48 nonresponders and 20 subjects naive to the HBV vaccine received a double dose of combined hepatitis A and B vaccine (Twinrix) at 0, 1, and 6 months. The levels of anti-HBs and antibodies to hepatitis A virus (anti-HAV) were determined before vaccination and 1 month after each dose.

    RESULTS: Among 44 nonresponders, protective anti-HBs levels were found in 26 (59%) after the first dose and in 42 (95%) after the third dose. Among the control subjects, the corresponding figures were 10% and 100%, respectively. All subjects seroconverted to anti-HAV. The titers of both anti-HBs and anti-HAV were lower in the previously nonresponsive subjects (P< .01).

    CONCLUSION: Revaccination of nonresponders to the standard hepatitis B vaccine regimen with a double dose of the combined hepatitis A and B vaccine was highly effective. This is most likely explained by the increased dose, a positive bystander effect conferred by the hepatitis A vaccine, or both.

  • 11.
    Carlsson, Björn
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi, Enheten för klinisk immunologi.
    Hou, Mingyan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi, Enheten för klinisk immunologi.
    Giandomenico, Valeria
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi, Enheten för klinisk immunologi.
    Nilsson, Berith
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi, Enheten för klinisk immunologi.
    Tötterman, Thomas H.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi.
    Essand, Magnus
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi, Enheten för klinisk immunologi.
    Simultaneous generation of cytomegalovirus-specific CD8+ and CD4+ T lymphocytes by use of dendritic cells comodified with pp65 mRNA and pp65 protein2005Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 192, nr 11, s. 1912-20Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Cytomegalovirus (CMV) disease remains a severe complication in patients who have undergone transplantation. Viremia can be prevented and treated by the adoptive transfer of donor-derived CMV-directed T cells. To ensure long-term protection against CMV disease, it is important to transfer CMV antigen-specific T cells that represent both the CD8+ and the CD4+ subsets. In the present study, we used as stimulators dendritic cells (DCs) that were electroporated with in vitro-transcribed 5'-capped polyadenylated messenger RNA (mRNA) that encoded the CMV pp65 protein (i.e., pp65 mRNA). These DCs could efficiently activate CMV-directed CD8+ T cells, as assayed by tetramer staining, interferon- gamma production, and cytolytic activity. We also used DCs that were pulsed with a recombinant pp65 protein to activate CMV-directed CD4+ T cells. When DCs were comodified with pp65 mRNA and pp65 protein, large numbers of CMV-directed CD8+ and CD4+ T cells were generated simultaneously. The approach outlined in the present study can be adapted for a clinical protocol that circumvents potential virus-related biohazards and is available to all patients independently of their human leukocyte antigen haplotype.

  • 12. Charpentier, E
    et al.
    Gerbaud, G
    Jacquet, C
    Rocourt, J
    Courvalin, P
    Incidence of antibiotic resistance in Listeria species.1995Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 172, nr 1, s. 277-281Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    To define the prevalence of antibiotic resistance in Listeria species pathogenic for humans and animals, 1100 isolates (60 from cases of listeriosis and 1040 from food and environment) collected worldwide were screened. Of the 61 tetracycline- and minocycline-resistant strains (37 Listeria monocytogenes), 57 harbored tet(M); 4 non-L. monocytogenes isolates contained tet(S). One Listeria innocua isolate was also resistant to streptomycin and contained the tet(M) and aad6 genes. An L. monocytogenes isolate was trimethoprim-resistant, a characteristic not reported previously in Listeria species, because of the presence of a yet-uncharacterized gene. Three clinical isolates of L. monocytogenes were resistant to low levels of streptomycin. Since the tet(M), tet(S), and aad6 genes are common in enterococci and streptococci, these data suggest transfer from the latter to Listeria species. Uniform susceptibility to tetracycline, minocycline, trimethoprim, and streptomycin cannot be assumed any longer for Listeria species.

  • 13. Chu, Y K
    et al.
    Jennings, G
    Schmaljohn, A
    Elgh, Fredrik
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Virologi.
    Hjelle, B
    Lee, H W
    Jenison, S
    Ksiazek, T
    Peters, C J
    Rollin, P
    Cross-neutralization of hantaviruses with immune sera from experimentally infected animals and from hemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome patients.1995Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 172, nr 6, s. 1581-4Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Plaque-reduction neutralization tests were done with eight of nine known representative hantaviruses and immune sera from experimentally infected animals and from patients with hemorrhagic fever with renal syndrome (HFRS) or hantavirus pulmonary syndrome (HPS). Results obtained with animal sera demonstrated each virus to be antigenically unique. Neutralization with the HPS patient sera was highest with Sin Nombre (SN) virus and to a lesser extent with Black Creek Canal (BCC) virus. Sera from Korean HFRS patients reacted best with Hantaan virus, but cross-reactivity with all other viruses except Thottapalayam (TPM) virus was also observed. Sera from Swedish HFRS patients reacted best with Puumala virus but cross-reacted with Prospect Hill, SN, and BCC viruses and to a lesser extent with all of the other viruses except TPM virus.

  • 14.
    Connolly-Andersen, Anne-Marie
    et al.
    Umeå University, Umeå, Sweden.
    Sundberg, Erik
    Umeå University, Umeå, Sweden.
    Ahlm, Clas
    Umeå University, Umeå, Sweden.
    Hultdin, Johan
    Umeå University, Umeå, Sweden.
    Baudin, Maria
    Umeå University, Umeå, Sweden.
    Larsson, Johanna
    Umeå University, Umeå, Sweden.
    Dunne, Eimear
    Royal Coll Surgeons Ireland, Dublin, Ireland.
    Kenny, Dermot
    Royal Coll Surgeons Ireland, Dublin, Ireland.
    Lindahl, Tomas L.
    Linköping University, Linköping, Sweden.
    Ramström, Sofia
    Linköping University, Linköping, Sweden.
    Nilsson, Sofie
    Umeå University, Umeå, Sweden.
    Increased Thrombopoiesis and Platelet Activation in Hantavirus-Infected Patients2015Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 212, nr 7, s. 1061-1069Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Thrombocytopenia is a common finding during viral hemorrhagic fever, which includes hemorrhagic fever with renal syndrome (HFRS). The 2 main causes for thrombocytopenia are impaired thrombopoiesis and/or increased peripheral destruction of platelets. In addition, there is an increased intravascular coagulation risk during HFRS, which could be due to platelet activation.

    Methods: Thrombopoiesis was determined by quantification of platelet counts, thrombopoietin, immature platelet fraction, and mean platelet volume during HFRS. The in vivo platelet activation was determined by quantification of soluble P-selectin (sP-selectin) and glycoprotein VI (sGPVI). The function of circulating platelets was determined by ex vivo stimulation followed by flow cytometry analysis of platelet surface-bound fibrinogen and P-selectin exposure. Intravascular coagulation during disease was determined by scoring for disseminated intravascular coagulation (DIC) and recording thromboembolic complications.

    Results: The levels of thrombopoietin, immature platelet fraction, and mean platelet volume all indicate increased thrombopoiesis during HFRS. Circulating platelets had reduced ex vivo function during disease compared to follow-up. Most interestingly, we observed significantly increased in vivo platelet activation in HFRS patients with intravascular coagulation (DIC and thromboembolic complications) as shown by sP-selectin and sGPVI levels. Conclusions. HFRS patients have increased thrombopoiesis and platelet activation, which contributes to intravascular coagulation.

  • 15.
    Connolly-Andersen, Anne-Marie
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Virologi. Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Sundberg, Erik
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Klinisk kemi. Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Ahlm, Clas
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Hultdin, Johan
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Klinisk kemi.
    Baudin, Maria
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Larsson, Johanna
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Klinisk kemi.
    Dunne, Eimear
    Clinical Research Centre, Royal College of Surgeons in Ireland, Dublin .
    Kenny, Dermot
    Clinical Research Centre, Royal College of Surgeons in Ireland, Dublin .
    Lindahl, Tomas L.
    Department of Clinical and Experimental Medicine, Linköping University, Sweden.
    Ramström, Sofia
    Department of Clinical and Experimental Medicine, Linköping University, Sweden.
    Nilsson, Sofie
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Klinisk kemi.
    Increased Thrombopoiesis and Platelet Activation in Hantavirus-Infected Patients2015Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 212, nr 7, s. 1061-1069Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background. Thrombocytopenia is a common finding during viral hemorrhagic fever, which includes hemorrhagic fever with renal syndrome (HFRS). The 2 main causes for thrombocytopenia are impaired thrombopoiesis and/or increased peripheral destruction of platelets. In addition, there is an increased intravascular coagulation risk during HFRS, which could be due to platelet activation. Methods. Thrombopoiesis was determined by quantification of platelet counts, thrombopoietin, immature platelet fraction, and mean platelet volume during HFRS. The in vivo platelet activation was determined by quantification of soluble P-selectin (sP-selectin) and glycoprotein VI (sGPVI). The function of circulating platelets was determined by ex vivo stimulation followed by flow cytometry analysis of platelet surface-bound fibrinogen and P-selectin exposure. Intravascular coagulation during disease was determined by scoring for disseminated intravascular coagulation (DIC) and recording thromboembolic complications. Results. The levels of thrombopoietin, immature platelet fraction, and mean platelet volume all indicate increased thrombopoiesis during HFRS. Circulating platelets had reduced ex vivo function during disease compared to follow-up. Most interestingly, we observed significantly increased in vivo platelet activation in HFRS patients with intravascular coagulation (DIC and thromboembolic complications) as shown by sP-selectin and sGPVI levels. Conclusions. HFRS patients have increased thrombopoiesis and platelet activation, which contributes to intravascular coagulation.

  • 16.
    Connolly-Andersen, Anne-Marie
    et al.
    Umeå University, Sweden.
    Sundberg, Erik
    Umeå University, Sweden.
    Ahlm, Clas
    Umeå University, Sweden.
    Hultdin, Johan
    Umeå University, Sweden.
    Baudin, Maria
    Umeå University, Sweden.
    Larsson, Johanna
    Umeå University, Sweden.
    Dunne, Eimear
    Royal Coll Surgeons Ireland, Ireland.
    Kenny, Dermot
    Royal Coll Surgeons Ireland, Ireland.
    Lindahl, Tomas
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Diagnostikcentrum, Klinisk kemi.
    Ramström, Sofia
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Medicinska fakulteten.
    Nilsson, Sofie
    Umeå University, Sweden.
    Increased Thrombopoiesis and Platelet Activation in Hantavirus-Infected Patients2015Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 212, nr 7, s. 1061-1069Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background. Thrombocytopenia is a common finding during viral hemorrhagic fever, which includes hemorrhagic fever with renal syndrome (HFRS). The 2 main causes for thrombocytopenia are impaired thrombopoiesis and/or increased peripheral destruction of platelets. In addition, there is an increased intravascular coagulation risk during HFRS, which could be due to platelet activation. Methods. Thrombopoiesis was determined by quantification of platelet counts, thrombopoietin, immature platelet fraction, and mean platelet volume during HFRS. The in vivo platelet activation was determined by quantification of soluble P-selectin (sP-selectin) and glycoprotein VI (sGPVI). The function of circulating platelets was determined by ex vivo stimulation followed by flow cytometry analysis of platelet surface-bound fibrinogen and P-selectin exposure. Intravascular coagulation during disease was determined by scoring for disseminated intravascular coagulation (DIC) and recording thromboembolic complications. Results. The levels of thrombopoietin, immature platelet fraction, and mean platelet volume all indicate increased thrombopoiesis during HFRS. Circulating platelets had reduced ex vivo function during disease compared to follow-up. Most interestingly, we observed significantly increased in vivo platelet activation in HFRS patients with intravascular coagulation (DIC and thromboembolic complications) as shown by sP-selectin and sGPVI levels. Conclusions. HFRS patients have increased thrombopoiesis and platelet activation, which contributes to intravascular coagulation.

  • 17.
    Cunningham, Anthony L.
    et al.
    Univ Sydney, Westmead Inst Med Res, Sydney, NSW, Australia.
    Heineman, Thomas C.
    GSK, King Of Prussia, PA USA;Genocea Biosci, Cambridge, MA USA.
    Lal, Himal
    GSK, King Of Prussia, PA USA;Pfizer Inc, Collegeville, PA USA.
    Godeaux, Olivier
    GSK, Wavre, Belgium;Janssen Vaccines & Prevent, Leiden, Netherlands.
    Chlibek, Roman
    Univ Def, Fac Mil Hlth Sci, Hradec Kralove, Czech Republic.
    Hwang, Shinn-Jang
    Taipei Vet Gen Hosp, Dept Family Med, Taipei, Taiwan;Natl Yang Ming Univ, Sch Med, Taipei, Taiwan.
    McElhaney, Janet E.
    Hlth Sci North Res Inst, Sudbury, ON, Canada.
    Vesikari, Timo
    Univ Tampere, Vaccine Res Ctr, Tampere, Finland.
    Andrews, Charles
    Diagnost Res Grp, San Antonio, TX USA.
    Choi, Won Suk
    Korea Univ, Coll Med, Dept Internal Med, Div Infect Dis, Seoul, South Korea.
    Esen, Meral
    Univ Clin Tuebingen, Inst Trop Med, Tubingen, Germany.
    Ikematsu, Hideyuki
    Japan Phys Assoc, Chiyoda Ku, Tokyo, Japan.
    Choma, Martina Kovac
    GSK, Rockville, MD USA.
    Pauksen, Karlis
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Infektionssjukdomar.
    Ravault, Stephanie
    GSK, Rixensart, Belgium.
    Salaun, Bruno
    GSK, Rixensart, Belgium.
    Schwarz, Tino F.
    Standort Juliusspital, Klinikum Wurzburg Mitte, Cent Lab & Vaccinat Ctr, Wurzburg, Germany.
    Smetana, Jan
    Univ Def, Fac Mil Hlth Sci, Hradec Kralove, Czech Republic.
    Vanden Abeele, Carline
    GSK, Wavre, Belgium.
    Van den Steen, Peter
    GSK, Wavre, Belgium.
    Vastiau, Ilse
    GSK, Wavre, Belgium.
    Weckx, Lily Yin
    Univ Fed Sao Paulo, Sao Paulo, Brazil.
    Levin, Myron J.
    Univ Colorado, Dept Pediat, Anschutz Med Campus, Aurora, CO USA;Univ Colorado, Dept Med, Anschutz Med Campus, Aurora, CO USA.
    Immune Responses to a Recombinant Glycoprotein E Herpes Zoster Vaccine in Adults Aged 50 Years or Older2018Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 217, nr 11, s. 1750-1760Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background. The herpes zoster subunit vaccine (HZ/su), consisting of varicella-zoster virus glycoprotein E (gE) and AS01(B) Adjuvant System, was highly efficacious in preventing herpes zoster in the ZOE-50 and ZOE-70 trials. We present immunogenicity results from those trials. Methods. Participants (ZOE-50: >= 50; ZOE-70: >= 70 years of age) received 2 doses of HZ/su or placebo, 2 months apart. Serum anti-gE antibodies and CD4 T cells expressing >= 2 of 4 activation markers assessed (CD4(2+)) after stimulation with gE-peptides were measured in subcohorts for humoral (n = 3293) and cell-mediated (n = 466) immunogenicity. Results. After vaccination, 97.8% of HZ/su and 2.0% of placebo recipients showed a humoral response. Geometric mean anti-gE antibody concentrations increased 39.1-fold and 8.3-fold over baseline in HZ/su recipients at 1 and 36 months post-dose 2, respectively. A gE-specific CD4(2+) T-cell response was shown in 93.3% of HZ/su and 0% of placebo recipients. Median CD42+ T-cell frequencies increased 24.6-fold (1 month) and 7.9-fold (36 months) over baseline in HZ/su recipients and remained >= 5.6-fold above baseline in all age groups at 36 months. The proportion of CD4 T cells expressing all 4 activation markers increased over time in all age groups. Conclusions. Most HZ/su recipients developed robust immune responses persisting for 3 years following vaccination.

  • 18. Dahl, Helena
    et al.
    Fjaertoft, Gustav
    Norsted, Torgny
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kvinnors och barns hälsa.
    Wang, Fu-Zhang
    Mousavi-Jazi, Merhdad
    Linde, Annika
    Reactivation of human herpesvirus 6 during pregnancy1999Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 180, nr 6, s. 2035-2038Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Reactivation of human herpesvirus 6 (HHV-6) and cytomegalovirus (CMV) during pregnancy and transmission of the viruses to the fetus were investigated by polymerase chain reaction (PCR) and serology. In all, 104 blood samples were obtained 3 times during pregnancy and once at delivery. In another 107 women, samples were obtained only at delivery. Cord blood samples were obtained from both groups of women. HHV-6 DNA was detected in 41%-44% of the samples during months 3-8 of pregnancy, in 25% at delivery, and in 24% of age-matched controls. HHV-6 DNA was found in 1.0% of the cord blood samples. CMV DNA was detected in 1.7% of leukocytes from 104 pregnant women but in no cord blood sample. IgG antibodies to HHV-6 were found in 96% and CMV IgG in 62.5% of the women. HHV-6 IgG titers were significantly higher in HHV-6 PCR-positive women. Thus, HHV-6 reactivation seems common during pregnancy, and transfer of HHV-6 to the fetus may occur in approximately 1% of pregnancies.

  • 19.
    Eklund, Daniel
    et al.
    Division of Microbiology and Molecular Medicine, Linköping University, Linköping, Sweden.
    Welin, Amanda
    Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Andersson, Henrik
    Division of Microbiology and Molecular Medicine, Linköping University, Linköping, Sweden.
    Verma, Deepti
    Division of Cell Biology, Faculty of Health Sciences, Linköping University, Linköping, Sweden.
    Söderkvist, Peter
    Division of Cell Biology, Faculty of Health Sciences, Linköping University, Linköping, Sweden.
    Stendahl, Olle
    Division of Microbiology and Molecular Medicine, Linköping University, Linköping, Sweden.
    Särndahl, Eva
    Örebro universitet, Institutionen för läkarutbildning.
    Lerm, Maria
    Division of Microbiology and Molecular Medicine, Linköping University, Linköping, Sweden.
    Human Gene Variants Linked to Enhanced NLRP3 Activity Limit Intramacrophage Growth of Mycobacterium tuberculosis2014Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 209, nr 5, s. 749-753Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Activation of the NLRP3 inflammasome and subsequent generation of interleukin 1 beta is initiated in macrophages upon recognition of several stimuli. In the present work, we show that gain-of-function gene variants of inflammasome components known to predispose individuals to inflammatory disorders have a host-protective role during infection with Mycobacterium tuberculosis. By isolation of macrophages from patients and healthy blood donors with genetic variants in NLRP3 and CARD8 and subsequent infection of the cells with virulent M. tuberculosis, we show that these gene variants, combined, are associated with increased control of bacterial growth in human macrophages.

  • 20.
    Elkington, Paul
    et al.
    Univ Southampton, England.
    Lerm, Maria
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi, infektion och inflammation. Linköpings universitet, Medicinska fakulteten.
    Kapoor, Nidhi
    Florida Hosp Adventist Hlth Syst, FL USA.
    Mahon, Robert
    NIAID, MD 20892 USA.
    Pienaar, Elsje
    Purdue Univ, IN 47907 USA.
    Huh, Dongeun
    Univ Penn, PA 19104 USA.
    Kaushal, Deepak
    Texas Biomed Res Inst, TX USA.
    Schlesinger, Larry S.
    Texas Biomed Res Inst, TX USA.
    In Vitro Granuloma Models of Tuberculosis: Potential and Challenges2019Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 219, nr 12, s. 1858-1866Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Despite intensive research efforts, several fundamental disease processes for tuberculosis (TB) remain poorly understood. A central enigma is that host immunity is necessary to control disease yet promotes transmission by causing lung immunopathology. Our inability to distinguish these processes makes it challenging to design rational novel interventions. Elucidating basic immune mechanisms likely requires both in vivo and in vitro analyses, since Mycobacterium tuberculosis is a highly specialized human pathogen. The classic immune response is the TB granuloma organized in three dimensions within extracellular matrix. Several groups are developing cell culture granuloma models. In January 2018, NIAID convened a workshop, entitled "3-D Human in vitro TB Granuloma Model" to advance the field. Here, we summarize the arguments for developing advanced TB cell culture models and critically review those currently available. We discuss how integrating complementary approaches, specifically organoids and mathematical modeling, can maximize progress, and conclude by discussing future challenges and opportunities.

  • 21. Frey, Sharon
    et al.
    Dagan, Ron
    Ashur, Yaffa
    Chen, Xiao Q.
    Ibarra, Jose
    Kollaritsch, Herwig
    Mazur, Mark H.
    Poland, Gregory A.
    Reisinger, Keith
    Walter, Emmanuel
    Van Damme, Pierre
    Braconier, Mark M.
    Uhnoo, Ingrid
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Wahl, Martin
    Blatter, Mark M.
    Clements, Dennis
    Greenberg, David
    Jacobson, Robert M.
    Norrby, S. Ragnar
    Rowe, Mina
    Shouval, Daniel
    Simmons, Sue S.
    van Hattum, Jan
    Wennerholm, Solveig
    Gress, Jacqueline O'Brien
    Chan, Ivan
    Kuter, Barbara
    Interference of antibody production to hepatitis B surface antigen in a combination hepatitis A/hepatitis B vaccine1999Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 180, nr 6, s. 2018-2022Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    A randomized trial comparing 3 manufacturing consistency lots of a combination hepatitis A/hepatitis B vaccine to each other and to hepatitis A vaccine and hepatitis B vaccine given separately and concurrently was done to evaluate safety, tolerability, and immunogenicity. Healthy volunteers >/=11 years of age were divided into 4 groups. Each of 3 groups received a separate consistency lot of the combination vaccine, and 1 group received separate but concurrent injections of hepatitis A and hepatitis B vaccines. Injections were given at weeks 0 and 24. The combination vaccine was generally well tolerated. The hepatitis A portion of the combination vaccine produced clinically acceptable high seropositivity rates 4 and 52 weeks after the first injection. The hepatitis B portion of the vaccine did not produce clinically acceptable seropositivity rates 4 weeks after the second injection. Lack of antibody production may be attributed, at least in part, to immunologic interference.

  • 22. Färnert, Anna
    et al.
    Williams, Thomas N.
    Mwangi, Tabitha W.
    Ehlin, Anna
    Fegan, Greg
    Macharia, Alex
    Lowe, Brett S.
    Montgomery, Scott M.
    Örebro universitet, Hälsoakademin.
    Marsh, Kevin
    Transmission-dependent tolerance to multiclonal Plasmodium falciparum infection2009Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 200, nr 7, s. 1166-1175Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Whether the number of concurrent clones in asymptomatic Plasmodium falciparum infections reflects the degree of host protection was investigated in children living in areas with different levels of transmission on the coast of Kenya. The number of concurrent clones was determined on the basis of polymorphism in msp2, which encodes the vaccine candidate antigen merozoite surface protein 2. In a low-transmission area, most children had monoclonal infections, and diversity did not predict a risk of clinical malaria. In an area of moderate transmission, asymptomatic infections with 2 clones were, compared with 1 clone, associated with an increased risk of subsequent malaria. In a comparative assessment in a high-transmission area in Tanzania, multiclonal infections conferred a reduced risk. The different nonlinear associations between the number of clones and malaria morbidity suggest that levels of tolerance to multiclonal infections are transmission dependent as a result of cumulative exposure to antigenically diverse P. falciparum infections.

  • 23.
    Gekara, Nelson O
    et al.
    Molecular Immunology, Helmholtz Centre for Infection Research, Braunschweig, Germany.
    Dietrich, Nicole
    Lyszkiewicz, Marcin
    Lienenklaus, Stefan
    Weiss, Siegfried
    Signals triggered by a bacterial pore-forming toxin contribute to toll-like receptor redundancy in gram-positive bacterial recognition.2009Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 199, nr 1, s. 124-33Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The results illustrate that signals triggered by LLO contribute to TLR2 redundancy in recognition of L. monocytogenes. Under normal conditions, multiple and, sometimes, redundant pathways cooperate to induce a rapid antimicrobial defense. When one signaling pathway-in this case, TLR2-is removed from the system, the other pathways are still capable of mounting a sufficient response to ensure survival of the host.

  • 24.
    Gekara, Nelson O
    et al.
    Molecular Immunology, Helmholtz Center for Infection Research, Braunschweig, Germany.
    Zietara, Natalia
    Molecular Immunology and 2Department of Cell Biology, Helmholtz Center for Infection Research, Braunschweig, Germany.
    Geffers, Robert
    Molecular Immunology and 2Department of Cell Biology, Helmholtz Center for Infection Research, Braunschweig, Germany.
    Weiss, Siegfried
    Molecular Immunology and 2Department of Cell Biology, Helmholtz Center for Infection Research, Braunschweig, Germany.
    Listeria monocytogenes induces T cell receptor unresponsiveness through pore-forming toxin listeriolysin O2010Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 202, nr 11, s. 1698-1707Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background.  The success of many pathogens relies on their ability to circumvent the innate and adaptive immune defenses. How bacterial pathogens subvert adaptive immune defenses is not clear. Cholesterol-dependent cytolysins (CDCs) represent an expansive family of homologous pore-forming toxins that are produced by more than 20 gram-positive bacterial species. Listeriolysin O (LLO), a prototype CDC, is the main virulence factor of Listeria monocytogenes. Methods.  We employed flow cytometric and microarray techniques to analyze the effect of LLO on T cell activation in vitro and in vivo. Results.  In vivo and in vitro proliferation of CD4(+) T cells upon T cell receptor (TCR) activation was highly diminished in the presence of LLO or wild-type L. monocytogenes but not in the presence of LLO-deficient L. monocytogenes. This block in T cell proliferation was specific to T cell activation via the TCR and not by phorbol 12-myristate 13-acetate-ionomycin, which bypasses the proximal TCR signaling event. The results of microarray analysis suggest that LLO-induced T cell unresponsiveness is due to the induction of a calcium-nuclear factor of activated T cells-dependent transcriptional program that drives the expression of negative regulators of TCR signaling. Conclusion. These findings provide important insights into how bacterial toxins silence adaptive immune responses and thus enable prolonged survival of the pathogen in the host.

  • 25.
    Geremariam Welearegay, Tesfalem
    et al.
    Rovira & Virgili Univ, Dept Elect Elect & Automat Engn, Tarragona, Spain.
    Diouani, Mohamed Fethi
    Univ Tunis El Manar, Lab Epidemiol & Vet Microbiol, Inst Pasteur Tunis, Tunis, Tunisia.
    Österlund, Lars
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Tekniska sektionen, Institutionen för teknikvetenskaper, Fasta tillståndets fysik. Mol Fingerprint AB Sweden, Uppsala, Sweden.
    Borys, Sebastian
    Univ Ctr Maritime & Trop Med, Gdynia Redlowo, Poland.
    Khaled, Samira
    Charles Nicolle Hosp, Parasitol Mycol Lab, Tunis, Tunisia.
    Smadhi, Hanen
    Abderrahman Mami Hosp, Ibn Nafis Pneumol Dept, Ariana, Tunisia.
    Ionescu, Florina
    Rovira & Virgili Univ, Dept Elect Elect & Automat Engn, Tarragona, Spain.
    Bouchekoua, Meriam
    Charles Nicolle Hosp, Parasitol Mycol Lab, Tunis, Tunisia.
    Aloui, Dorsaf
    Charles Nicolle Hosp, Parasitol Mycol Lab, Tunis, Tunisia.
    Laouini, Dhafer
    Univ Tunis El Manar, Lab Transmiss Control & Immunobiol Infect, Inst Pasteur Tunis, Tunis, Tunisia.
    Cindemir, Umut
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Tekniska sektionen, Institutionen för teknikvetenskaper, Fasta tillståndets fysik. Mol Fingerprint AB Sweden, Uppsala, Sweden.
    Ionescu, Radu
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Tekniska sektionen, Institutionen för teknikvetenskaper, Fasta tillståndets fysik. Rovira & Virgili Univ, Dept Elect Elect & Automat Engn, Tarragona, Spain;Inst Macromol Chem Petru Poni, Iasi, Romania.
    Diagnosis of Human Echinococcosis via Exhaled Breath Analysis: A Promise for Rapid Diagnosis of Infectious Diseases Caused by Helminths2019Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 219, nr 1, s. 101-109Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Human echinococcosis is a neglected infectious disease affecting more than 1 million people globally. Its diagnosis is expensive and difficult because of lack of adequate resources in low-resource locations, where most cases occur.

    Methods: A group of volunteers diagnosed with the 2 main types of echinococcosis and corresponding control groups were recruited from hospitals in Tunisia (32 patients with cystic echinococcosis and 43 controls) and Poland (16 patients with alveolar echinococcosis and 8 controls). Breath samples were collected from all patients and analyzed by gas chromatography coupled to mass spectrometry, and a specifically developed electronic nose system.

    Results: The chemical analysis revealed statistically different concentrations of 2 compounds in the breath of patients with cystic echinococcosis compared to controls, and statistically different concentrations of 7 compounds in the breath of patients with alveolar echinococcosis compared to controls. The discrimination accuracy achieved by the electronic nose system was 100% for cystic echinococcosis and 92.9% for alveolar echinococcosis, while the discrimination accuracy between these 2 patient groups was 92.1%.

    Conclusion: Here we advocate a noninvasive, fast, easy-to-operate and nonexpensive diagnostic tool for the diagnosis of human echinococcosis disease through exhaled breath analysis, suitable for early diagnosis and population screening.

  • 26. Gibbs, Anna
    et al.
    Buggert, Marcus
    Edfeldt, Gabriella
    Ranefall, Petter
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Matematisk-datavetenskapliga sektionen, Institutionen för informationsteknologi, Avdelningen för visuell information och interaktion. Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Matematisk-datavetenskapliga sektionen, Institutionen för informationsteknologi, Bildanalys och människa-datorinteraktion. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Introini, Andrea
    Cheuk, Stanley
    Martini, Elisa
    Eidsmo, Liv
    Ball, Terry B.
    Kimani, Joshua
    Kaul, Rupert
    Karlsson, Annika C.
    Wählby, Carolina
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Matematisk-datavetenskapliga sektionen, Institutionen för informationsteknologi, Avdelningen för visuell information och interaktion. Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Matematisk-datavetenskapliga sektionen, Institutionen för informationsteknologi, Bildanalys och människa-datorinteraktion. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Broliden, Kristina
    Tjernlund, Annelie
    Human Immunodeficiency Virus-Infected Women Have High Numbers of CD103-CD8+ T Cells Residing Close to the Basal Membrane of the Ectocervical Epithelium2018Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 218, nr 3, s. 453-465Artikel i tidskrift (Refereegranskat)
  • 27. Goncalves, Adriana
    et al.
    Peeling, Rosanna W.
    Chu, May C.
    Gubler, Duane J.
    de Silva, Aravinda M.
    Harris, Eva
    Murtagh, Maurine
    Chua, Arlene
    Rodriguez, William
    Kelly, Cassandra
    Wilder-Smith, Annelies
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Epidemiologi och global hälsa. Lee Kong Chian School of Medicine, Singapore; Institute of Public Health, University of Heidelberg, Germany.
    Innovative and New Approaches to Laboratory Diagnosis of Zika and Dengue: A Meeting Report2018Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 217, nr 7, s. 1060-1068Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Epidemics of dengue, Zika, and other arboviral diseases are increasing in frequency and severity. Current efforts to rapidly identify and manage these epidemics are limited by the short diagnostic window in acute infection, the extensive serologic cross-reactivity among flaviviruses, and the lack of point-of-care diagnostic tools to detect these viral species in primary care settings. The Partnership for Dengue Control organized a workshop to review the current landscape of Flavivirus diagnostic tools, identified current gaps, and developed strategies to accelerate the adoption of promising novel technologies into national programs. The rate-limiting step to bringing new diagnostic tools to the market is access to reference materials and well-characterized clinical samples to facilitate performance evaluation. We suggest the creation of an international laboratory-response consortium for flaviviruses with a decentralized biobank of well-characterized samples to facilitate assay validation. Access to proficiency panels are needed to ensure quality control, in additional to in-country capacity building.

  • 28.
    Gothefors, Leif
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Ahrén, C
    Stoll, B
    Barua, D K
    Orskov, F
    Salek, M A
    Svennerholm, A M
    Presence of colonization factor antigens on fresh isolates of fecal Escherichia coli: a prospective study.1985Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 152, nr 6, s. 1128-33Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    In Dhaka, Bangladesh, fresh isolates of Escherichia coli from 197 patients with diarrhea were investigated for production of enterotoxin and possession of colonization factor antigen (CFA) I or II. Enterotoxigenic E. coli (ETEC) was isolated from 34% of the patients, and of the 67 enterotoxin-positive strains, 75% carried CFAs. Among 68 healthy control persons no strains positive for both enterotoxin and CFA were found. The CFAs in general were restricted to certain serotypes of E. coli. In a subgroup of patients, part of an ongoing surveillance study, mixed infection was seen in 23% of those from whom recognized pathogens were identified. There was a tendency to more severe dehydration when the two virulence factors, enterotoxin and CFA, were simultaneously present.

  • 29.
    Gothefors, Leif
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Wadell, G
    Juto, P
    Taniguchi, K
    Kapikian, A Z
    Glass, R I
    Prolonged efficacy of rhesus rotavirus vaccine in Swedish children.1989Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 159, nr 4, s. 753-7Artikel i tidskrift (Refereegranskat)
  • 30. Grankvist, Olof
    et al.
    Juto, Per
    Settergren, Bo
    Ahlm, Clas
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Bjermer, L
    Linderholm, M
    Tärnvik, A
    Wadell, G
    Detection of nephropathia epidemica virus RNA in patient samples using a nested primer-based polymerase chain reaction.1992Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 165, nr 5, s. 934-7Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    A nested primer-based polymerase chain reaction was constructed for the detection of Puumala virus RNA in patient samples. Puumala virus RNA was detected in cells from the urinary and the respiratory tracts and in peripheral blood mononuclear cells of patients with nephropathia epidemica. After inoculation with nephropathia epidemica patient material on Vero E6 cells and propagation for nine passages (4 months), Puumala virus RNA was detected at every passage. Hybridization under high-stringency conditions revealed that the overall nucleotide homology between the different patient isolates and the prototype strain (Puumala) is high. Using cDNA from Hällnäs B1 strain as a probe, hybridization occurred only under low-stringency conditions.

  • 31.
    Günaydın, Gökçe
    et al.
    Division of Clinical Immunology, Karolinska Institutet at Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Nordgren, Johan
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin.
    Svensson, Lennart
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin.
    Hammarström, Lennart
    Division of Clinical Immunology, Karolinska Institutet at Karolinska University Hospital Huddinge, Stockholm, Sweden.
    TLR3-dependent antibody response against rotavirus in individuals with immunoglobulin A deficiency2013Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613Artikel i tidskrift (Refereegranskat)
  • 32. Hammerschlag, Margaret R
    et al.
    Apfalter, Petra
    Boman, Jens
    Umeå universitet, Medicinsk fakultet, Klinisk mikrobiologi, Virologi.
    Tondella, M Lucia
    Gaydos, Charlotte
    The role of Chlamydia pneumoniae in multiple sclerosis: real or fictitious?2005Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 192, nr 7, s. 1305-7; author reply 1307Artikel i tidskrift (Refereegranskat)
  • 33. Hanevik, Kurt
    et al.
    Kristoffersen, Einar
    Svärd, Staffan
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi, Mikrobiologi.
    Bruserud, Oystein
    Ringqvist, Emma
    Sornes, Steinar
    Langeland, Nina
    Human Cellular Immune Response Against Giardia lamblia 5 Years After Acute Giardiasis2011Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 204, nr 11, s. 1779-1786Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background. Clinical and epidemiological studies have suggested the development of acquired immunity in individuals previously infected with Giardia lamblia. However, there are no data on the long-term cellular immunity and genotype cross-reactivity. An outbreak of assemblage B giardiasis in a nonendemic area made it possible to evaluate the long-term cellular mediated immunity and its specificity toward the 2 Giardia assemblages known to infect humans.

    Methods. Peripheral blood mononuclear cells from 19 individuals infected with Giardia assemblage B 5 years previously and from 10 uninfected controls were cultured with antigens from assemblage A and B Giardia trophozoites for 6 days. Cell-mediated immunity was measured by a (3)H-thymidine proliferation assay and flow cytometric analysis of activation markers HLA-DR, CD45RO, CD25, and CD26 in T-cell subsets.

    Results. Proliferation responses were significantly elevated in the group previously exposed to Giardia for nearly all Giardia antigens tested. Individual responses toward Giardia trophozoite whole cell, cytosolic, and excretory-secretory antigens from both assemblages correlated well. Activation marker responses were mainly seen in CD4 T cells.

    Conclusions. G. lamblia infection induces long-term, albeit variable, cellular immune responses that are not assemblage specific and that are largely driven by CD4 T-cell activation.

  • 34. Henningsson, Louise
    et al.
    Jirholt, Pernilla
    Bogestal, Yalda Rahpeymai
    Eneljung, Tove
    Adiels, Martin
    Lindholm, Catharina
    McInnes, Iain
    Bulfone-Paus, Silvia
    Lerner, Ulf H
    Umeå universitet, Medicinska fakulteten, Institutionen för odontologi, Molekylär paradontologi.
    Gjertsson, Inger
    Interleukin 15 mediates joint destruction in staphylococcus aureus arthritis2012Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 206, nr 5, s. 687-696Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background. Staphylococcus aureus arthritis causes severe and rapid joint damage despite antibiotics. Thus, there is a need to identify new treatment targets in addition to antibiotics. Lately, interleukin 15 (IL-15) has been implicated both in osteoclastogenesis and in bacterial clearance-2 important issues in S. aureus-induced joint destruction. This has prompted us to investigate the importance of IL-15 in S. aureus-induced arthritis.

    Methods.Toxic shock syndrome toxin-1 producing S. aureus was intravenously inoculated in IL-15 knockout and wildtype mice and in wildtype mice treated with anti-IL-15 antibodies (aIL-15ab) or isotype control antibody.

    Results. Absence of IL-15, either in knockout mice or after treatment with aIL-15ab, significantly reduced weight loss compared with controls during the infection. The severity of synovitis and joint destruction was significantly decreased in IL-15 knockout and aIL-15ab treated mice compared with controls. In IL-15 knockout mice there was a reduced number of osteoclasts in the joints. The host's ability to clear bacteria was not influenced in the IL-15 knockout mice, but significantly increased after treatment with aIL-15ab.

    Conclusions. IL-15 is a mediator of joint destruction in S. aureus-induced arthritis and contributes to general morbidity, which makes this cytokine an interesting treatment target in addition to conventional antibiotics.

  • 35. Howard, Jennifer
    et al.
    Loizon, Séverine
    Tyler, Christopher J.
    Duluc, Dorothée
    Moser, Bernhard
    Mechain, Matthieu
    Duvignaud, Alexandre
    Malvy, Denis
    Troye-Blomberg, Marita
    Stockholms universitet, Naturvetenskapliga fakulteten, Institutionen för molekylär biovetenskap, Wenner-Grens institut.
    Moreau, Jean-Francois
    Eberl, Matthias
    Mercereau-Puijalon, Odile
    Déchanet-Merville, Julie
    Behr, Charlotte
    Mamani-Matsuda, Maria
    The Antigen-Presenting Potential of V gamma 9V delta 2 T Cells During Plasmodium falciparum Blood-Stage Infection2017Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 215, nr 10, s. 1569-1579Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    During Plasmodium falciparum infections, erythrocyte-stage parasites inhibit dendritic cell maturation and function, compromising effective antimalarial adaptive immunity. Human V gamma 9V delta 2 T cells can act in vitro as antigen-presenting cells (APCs) and induce alpha beta T-cell activation. However, the relevance of this activity in vivo has remained elusive. Because V gamma 9V delta 2 T cells are activated during the early immune response against P. falciparum infection, we investigated whether they could contribute to the instruction of adaptive immune responses toward malaria parasites. In P. falciparum-infected patients, V gamma 9V delta 2 T cells presented increased surface expression of APC-associated markers HLA-DR and CD86. In response to infected red blood cells in vitro, V gamma 9V delta 2 T cells upregulated surface expression of HLA-DR, HLA-ABC, CD40, CD80, CD83, and CD86, induced naive alpha beta T-cell responses, and cross-presented soluble prototypical protein to antigen-specific CD8(+) T cells. Our findings qualify V gamma 9V delta 2 T cells as alternative APCs, which could be harnessed for therapeutic interventions and vaccine design.

  • 36.
    Jacobsen, Marc
    et al.
    Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
    Repsilber, Dirk
    Institute for Medical Biometry and Statistics, University of Lübeck, Lübeck, Germany.
    Gutschmidt, Andrea
    Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
    Neher, Albert
    Asklepios Center for Respiratory Medicine and Thoracic Surgery, Munich-Gauting, Germany .
    Feldmann, Knut
    Asklepios Center for Respiratory Medicine and Thoracic Surgery, Munich-Gauting, Germany .
    Mollenkopf, Hans J
    Microarray Core Facilities, Max Planck Institute for Infection Biology, Berlin, Germany .
    Ziegler, Andreas
    Institute for Medical Biometry and Statistics, University of Lübeck, Lübeck, Germany.
    Kaufmann, Stefan H E
    Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
    Ras-associated small GTPase 33A, a novel T cell factor, is down-regulated in patients with tuberculosis2005Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 192, nr 7, s. 1211-8Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Ras-associated small GTPases (Rabs) are specific regulators of intracellular vesicle trafficking. Interference with host cell vesicular transport is a hallmark of many intracellular pathogens, including the notable example Mycobacterium tuberculosis. We performed, by quantitative polymerase chain reaction, gene-expression analyses for selected Rab molecules in peripheral-blood mononuclear cells from patients with tuberculosis (TB) and healthy control subjects, to identify candidate genes that are critically involved in the host immune response. Comparison revealed significant differences in the expression of genes for Rab13, Rab24, and Rab33A. Rab33A gene expression was down-regulated in patients with TB and was predominantly expressed in CD8+ T cells. We excluded possible influences of differences in T cell percentages between the 2 study groups, demonstrating that Rab33A gene expression changes on the single-cell level. In vitro, Rab33A RNA expression was induced in T cells on activation and by dendritic cells infected with M. tuberculosis. Our findings identify Rab33A as a T cell regulatory molecule in TB and suggest its involvement in disease processes.

  • 37.
    Kenyon, Chris
    et al.
    HIV/STI Unit, Institute of Tropical Medicine, Antwerp, Belgium; Division of Infectious Diseases and HIV Medicine, University of Cape Town, Anzio Road, Observatory, South Africa.
    Buyze, Jozefien
    Clinical Trials Unit, Institute of Tropical Medicine, Antwerp, Belgium.
    Spiteri, G.
    European Centre for Disease Prevention and Control, Stockholm, Sweden.
    Cole, M. J.
    National Infection Service, Public Health England, London, United Kingdom.
    Unemo, Magnus
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. WHO Collaborating Centre for Gonorrhoea and other Sexually Transmitted Infections, Department of Laboratory Medicine.
    Population-level antimicrobial consumption is associated with decreased antimicrobial susceptibility in Neisseria gonorrhoeae in 24 European countries: an ecological analysis2019Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, artikel-id jiz153Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    OBJECTIVES: There are substantial variations in Neisseria gonorrhoeae susceptibility to antimicrobials between different populations, and the reasons for this are largely unexplored. We aimed to assess if the population level consumption of antimicrobials is a contributory factor.

    METHODS: Using antimicrobial susceptibility data from 24 countries in the European Gonococcal Antimicrobial Surveillance Programme and antimicrobial consumption data from the IQVIA MIDAS database, we built mixed effects linear/logistic regression models with country-level cephalosporin, fluoroquinolone and macrolide consumption (standard doses/1000 population/year) as the explanatory variables (from 2009 to 2015) and 1-year lagged ceftriaxone, cefixime, azithromycin and ciprofloxacin geometric mean minimum inhibitory concentrations (MIC) as the outcome variables (2010 to 2016).

    RESULTS: Positive correlations were found between the consumption of cephalosporins and geometric mean MIC of ceftriaxone and cefixime (both P's <0.05). Fluoroquinolone consumption was positively associated with the prevalence of resistance to ciprofloxacin (P<0.05).

    CONCLUSIONS: Differences in population level consumption of particular antimicrobials may contribute to the variations in the level of antimicrobial resistance in N. gonorrhoeae in different settings. Further interventions to reduce misuse and overuse of antimicrobials in high-consumption populations and core-groups are required.

  • 38.
    Kindberg, Elin
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Molekylär virologi. Linköpings universitet, Hälsouniversitetet.
    Mickiene, Aukse
    Department of Medicine Karolinska University Hospital Huddinge.
    Ax, Cecilia
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Hälsouniversitetet.
    Åkerlind, Britt
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Klinisk mikrobiologi. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk mikrobiologi.
    Vene, Sirkka
    5Swedish Institute for Infectious Disease Control Karolinska Institutet, Stockholm.
    Lindquist, Lars
    Department of Medicine Karolinska University Hospital Huddinge.
    Lundkvist, Åke
    Swedish Institute for Infectious Disease Control Karolinska Institutet, Stockholm.
    Svensson, Lennart
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Molekylär virologi. Linköpings universitet, Hälsouniversitetet.
    A deletion in the chemokine receptor 5 (CCR5) gene is associated with tickborne encephalitis2008Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 197, nr 2, s. 266-269Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Tickborne encephalitis (TBE) virus infections can be asymptomatic or cause moderate to severe injuries of the central nervous system. Why some individuals develop severe disease is unknown, but a role for host genetic factors has been suggested. To investigate whether chemokine receptor CCR5 is associated with TBE, CCR5Δ32 genotyping was performed among Lithuanian patients with TBE (n = 129) or with aseptic meningoencephalitis (n = 76) as well as among control subjects (n = 134). We found individuals homozygous for CCR5Δ32 (P = .026) only among patients with TBE and a higher allele prevalence among patients with TBE compared with the other groups studied. CCR5Δ32 allele prevalence also increased with the clinical severity of disease. © 2007 by the Infectious Diseases Society of America. All rights reserved.

  • 39. Kubler, Andre
    et al.
    Larsson, Christer
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Luna, Brian
    Andrade, Bruno B.
    Amaral, Eduardo P.
    Urbanowski, Michael
    Orandle, Marlene
    Bock, Kevin
    Ammerman, Nicole C.
    Cheung, Laurene S.
    Winglee, Kathryn
    Halushka, Marc
    Park, Jin Kyun
    Sher, Alan
    Friedland, Jon S.
    Elkington, Paul T.
    Bishai, William R.
    Cathepsin K Contributes to Cavitation and Collagen Turnover in Pulmonary Tuberculosis2016Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 213, nr 4, s. 618-627Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Cavitation in tuberculosis enables highly efficient person-to-person aerosol transmission. We performed transcriptomics in the rabbit cavitary tuberculosis model. Among 17 318 transcripts, we identified 22 upregulated proteases. Five type I collagenases were overrepresented: cathepsin K (CTSK), mast cell chymase-1 (CMA1), matrix metalloproteinase 1 (MMP-1), MMP-13, and MMP-14. Studies of collagen turnover markers, specifically, collagen type I C-terminal propeptide (CICP), urinary deoxypyridinoline (DPD), and urinary helical peptide, revealed that cavitation in tuberculosis leads to both type I collagen destruction and synthesis and that proteases other than MMP-1, MMP-13, and MMP-14 are involved, suggesting a key role for CTSK. We confirmed the importance of CTSK upregulation in human lung specimens, using immunohistochemical analysis, which revealed perigranulomatous staining for CTSK, and we showed that CTSK levels were increased in the serum of patients with tuberculosis, compared with those in controls (3.3 vs 0.3 ng/mL; P = .005).

  • 40.
    Kwiecinski, J
    et al.
    Sahlgrenska Academy.
    Josefsson, E
    Sahlgrenska Academy.
    Mitchell, J
    Trinity College, Dublin.
    Higgins, J
    Trinity College, Dublin.
    Magnusson, Mattias
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Reumatologi. Linköpings universitet, Hälsouniversitetet.
    Foster, T
    Trinity College, Dublin.
    Jin, T
    Sahlgrenska Academy.
    Bokarewa, M
    Sahlgrenska Academy.
    Activation of Plasminogen by Staphylokinase Reduces the Severity of Staphylococcus aureusSystemic Systemic Infection2010Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 202, nr 7, s. 1041-1049Artikel i tidskrift (Refereegranskat)
    Abstract [en]

     

    Background. Theoretical and experimental data support the geographic differentiation strategy as a valuable tool for detecting loci under selection. In the context of Plasmodium falciparum malaria, few populations have been studied, with limited genomic coverage.

    Methods. Wild-type S. aureus strain LS-1, which lacks the ability to produce SAK, was modified by an insertion of the sak gene into its chromosome. The sak gene was integrated in 2 forms—(1) linked to its own promoter and (2) fused to the promoter of the protein A gene—which resulted in the overexpression of SAK. SAK is highly specific for human plg and exhibits almost no activity toward murine plg. To investigate the role played by SAK in a murine infection model, human plg transgenic mice and their wild-type counterparts were inoculated intravenously with congenic S. aureus strains differing in SAK production.

    Results. Human plg transgenic mice inoculated with SAK-expressing strains displayed significantly reduced mortality, less weight loss, and lower bacterial loads in kidneys than did the wild-type mice. No difference in the severity of sepsis was observed between transgenic and wild-type mice infected with a SAK-deficient strain.

    Conclusions. The results suggest that expression of SAK followed by activation of plg alleviates the course of S. aureus sepsis. 

     

     

     

     

     

     

     

     

     

      

     

     

     

     

     

     

     

     

     

     

     

     

     

    Background.

     

    Staphylokinase (SAK) is produced by the majority of Staphylococcus aureus strains. It is an extracellular protein that activates the conversion of human plasminogen (plg) to plasmin. The role played by SAK in staphylococcal infection is unclear.Methods. Wild-type S. aureus strain LS-1, which lacks the ability to produce SAK, was modified by an insertion of the sak gene into its chromosome. The sak gene was integrated in 2 forms—(1) linked to its own promoter and (2) fused to the promoter of the protein A gene—which resulted in the overexpression of SAK. SAK is highly specific for human plg and exhibits almost no activity toward murine plg. To investigate the role played by SAK in a murine infection model, human plg transgenic mice and their wild-type counterparts were inoculated intravenously with congenic S. aureus strains differing in SAK production.Results. Human plg transgenic mice inoculated with SAK-expressing strains displayed significantly reduced mortality, less weight loss, and lower bacterial loads in kidneys than did the wild-type mice. No difference in the severity of sepsis was observed between transgenic and wild-type mice infected with a SAK-deficient strain.Conclusions. The results suggest that expression of SAK followed by activation of plg alleviates the course of S. aureus

    sepsis.

  • 41. Kwiecinski, Jakub
    et al.
    Jacobsson, Gunnar
    Karlsson, Maria
    Zhu, Xuefeng
    Wang, Wanzhong
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap.
    Bremell, Tomas
    Josefsson, Elisabet
    Jin, Tao
    Staphylokinase Promotes the Establishment of Staphylococcus aureus Skin Infections While Decreasing Disease Severity2013Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 208, nr 6, s. 990-999Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Skin infections are frequently caused by Staphylococcus aureus and can lead to a fatal sepsis. The microbial mechanisms controlling the initiation and progression from mild skin infection to a severe disseminated infection remain poorly understood. Using a combination of clinical data and in vitro and ex vivo assays, we show that staphylokinase, secreted by S. aureus, promoted the establishment of skin infections in humans and increased bacterial penetration through skin barriers by activating plasminogen. However, when infection was established, the interaction between staphylokinase and plasminogen did not promote systemic dissemination but induced the opening and draining of abscesses and decreased disease severity in neutropenic mice. Also, increased staphylokinase production was associated with noninvasive S. aureus infections in patients. Our results point out the dual roles of staphylokinase in S. aureus skin infections as promoting the establishment of infections while decreasing disease severity.

  • 42. Lane, BR
    et al.
    Ast, Jennifer C
    University of Michigan, Museum of Zoology and Department of Biology.
    Hossler, PR
    Mindell, David P
    University of Michigan, Museum of Zoology and Department of Biology.
    Bartlett, MS
    Smith, JW
    Meshnik, SR
    University of Michigan.
    Dihydropteroate synthase polymorphisms in Pneumocystis carini1997Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 175, s. 483-485Artikel i tidskrift (Refereegranskat)
  • 43.
    Larsson, Christer
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
    Andersson, Marie
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
    Guo, Betty P
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
    Nordstrand, Annika
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
    Hägerstrand, Inga
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
    Carlsson, Sara
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
    Bergström, Sven
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
    Complications of pregnancy and transplacental transmission of relapsing-fever borreliosis2006Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 194, nr 10, s. 1367-1374Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Relapsing-fever borreliosis caused by Borrelia duttonii is a common cause of complications of pregnancy, miscarriage, and neonatal death in sub-Saharan Africa. We established a murine model of gestational relapsing fever infection for the study of the pathological development of these complications. We demonstrate that B. duttonii infection during pregnancy results in intrauterine growth retardation, as well as placental damage and inflammation, impaired fetal circulation, and decreased maternal hemoglobin levels. We show that spirochetes frequently cross the maternal-fetal barrier, resulting in congenital infection. Furthermore, we compared the severity of infection in pregnant and nonpregnant mice and show that pregnancy has a protective effect. This model closely parallels the consequences of human gestational infection, and our results provide insight into the mechanisms behind the complications of pregnancy that have been reported in human relapsing-fever infection.

  • 44.
    Linderholm, Mats
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Ahlm, Clas
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Settergren, Bo
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Waage, A
    Tärnvik, Arne
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Infektionssjukdomar.
    Elevated plasma levels of tumor necrosis factor (TNF)-alpha, soluble TNF receptors, interleukin (IL)-6, and IL-10 in patients with hemorrhagic fever with renal syndrome.1996Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 173, nr 1, s. 38-43Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Plasma levels of cytokines were measured by EIA in 15 subjects hospitalized with nephropathia epidemica, a European form of hantavirus-induced hemorrhagic fever with renal syndrome. Concentrations of tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 were increased in all patients at admission, and the concentration of IL-10 was increased in most. TNF-alpha concentrations were still increased 1 week after onset of disease; levels of IL-6 and IL-10 were normalized. TNF-alpha was undetectable by the WEHI cell assay in serum samples obtained throughout the acute phase of disease. Serum levels of the two soluble TNF receptors p55 and p75 correlated with levels of the cytokine, indicating that receptor binding may be the reason for lack of bioactivity in vitro. TNF-alpha is known to induce pathophysiologic and clinical changes similar to those seen in nephropathia epidemica and in diseases caused by other hantaviruses.

  • 45. Margeridon-Thermet, S
    et al.
    Shulman, NS
    Ahmed, A
    Shahriar, R
    Liu, T
    Wang, C
    Holmes, SP
    Babrzadeh, Farbod
    Stanford Genome Technology Centre, USA.
    Gharizadeh, B
    Hanczaruk, B
    Simen, BB
    Egholm, M
    Shafer, RW
    Ultra-deep pyrosequencing of hepatitis B virus quasispecies from nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI)-treated patients and NRTI-naive patients2009Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 199, nr 9, s. 1275-1285Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The dynamics of emerging nucleoside and nucleotide reverse-transcriptase inhibitor (NRTI) resistance in hepatitis B virus (HBV) are not well understood because standard dideoxynucleotide direct polymerase chain reaction (PCR) sequencing assays detect drug-resistance mutations only after they have become dominant. To obtain insight into NRTI resistance, we used a new sequencing technology to characterize the spectrum of low-prevalence NRTI-resistance mutations in HBV obtained from 20 plasma samples from 11 NRTI-treated patients and 17 plasma samples from 17 NRTI-naive patients, by using standard direct PCR sequencing and ultra-deep pyrosequencing (UDPS). UDPS detected drug-resistance mutations that were not detected by PCR in 10 samples from 5 NRTI-treated patients, including the lamivudine-resistance mutation V173L (in 5 samples), the entecavir-resistance mutations T184S (in 2 samples) and S202G (in 1 sample), the adefovir-resistance mutation N236T (in 1 sample), and the lamivudine and adefovir-resistance mutations V173L, L180M, A181T, and M204V (in 1 sample). G-to-A hypermutation mediated by the apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like family of cytidine deaminases was estimated to be present in 0.6% of reverse-transcriptase genes. Genotype A coinfection was detected by UDPS in each of 3 patients in whom genotype G virus was detected by direct PCR sequencing. UDPS detected low-prevalence HBV variants with NRTI-resistance mutations, G-to-A hypermutation, and low-level dual genotype infection with a sensitivity not previously possible.

  • 46. McCall, Matthew B B
    et al.
    Hopman, Joost
    Daou, Modibo
    Maiga, Boubacar
    Dara, Victor
    Ploemen, Ivo
    Nganou-Makamdop, Krystelle
    Niangaly, Amadou
    Tolo, Youssouf
    Arama, Charles
    Stockholms universitet, Naturvetenskapliga fakulteten, Wenner-Grens institut, Avdelningen för immunologi.
    Bousema, J Teun
    van der Meer, Jos W
    van der Ven, André J A M
    Troye-Blomberg, Marita
    Stockholms universitet, Naturvetenskapliga fakulteten, Wenner-Grens institut, Avdelningen för immunologi.
    Dolo, Amagana
    Doumbo, Ogobara K
    Sauerwein, Robert W
    Early interferon-gamma response against Plasmodium falciparum correlates with interethnic differences in susceptibility to parasitemia between sympatric Fulani and Dogon in Mali.2010Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 201, nr 1, s. 142-52Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    INTRODUCTION: Interethnic differences in susceptibility to malaria provide a unique opportunity to explore immunological correlates of protection. The Fulani of Sahelian Africa are known for their reduced susceptibility to Plasmodium falciparum, compared with surrounding tribes, yet the immunology underlying this is still poorly understood. METHODS AND RESULTS: Here, we show that mononuclear cells from Fulani elicit >10-fold stronger interferon (IFN)-gamma production following a 24-h in vitro coincubation with asexual parasites than cells from sympatric Dogon. This response appears to be specific for P. falciparum among a panel of other human pathogens and is independent of the lower number of regulatory T cell counts present in Fulani. IFN-gamma responses in both tribes were inversely correlated with peripheral parasite density as quantified by nucleic acid sequenced-based amplification, but responses of Fulani remained significantly stronger than those of Dogon after adjustment for concurrent parasitemia, suggesting that hard-wired immunological differences underlie the observed protection. CONCLUSIONS: These results underscore the value of early IFN-gamma responses to P. falciparum as a correlate of anti-parasite immunity, not only in this setting but also in the wider context of malaria, and support the development of malaria vaccines aimed at inducing such responses.

  • 47.
    Modin Larsson, Malin
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Molekylär virologi. Linköpings universitet, Hälsouniversitetet.
    Rydell, Gustaf
    Department of Clinical Chemistry and Transfusion Medicine, Sahlgrenska University Hospital, Göteborg.
    Grahn, Ammi
    Department of Clinical Chemistry and Transfusion Medicine, Sahlgrenska University Hospital, Göteborg.
    Rodríguez-Díaz, Jesús
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Molekylär virologi. Linköpings universitet, Hälsouniversitetet.
    Åkerlind, Britt
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Klinisk mikrobiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Diagnostikcentrum, Klinisk mikrobiologi.
    Hutson, Anne
    Departments of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas, USA .
    Estes, Mary
    Departments of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas, USA.
    Larson, Göran
    Department of Clinical Chemistry and Transfusion Medicine, Sahlgrenska University Hospital, Göteborg.
    Svensson, Lennart
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Molekylär virologi. Linköpings universitet, Hälsouniversitetet.
    Antibody Prevalence and Titer to Norovirus (Genogroup II) Correlate with Secretor (FUT2) but Not with ABO Phenotype or Lewis (FUT3) Genotype2006Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 194, nr 10, s. 1422-1427Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND:

    Histo-blood group antigens and secretor status have been associated with susceptibility to Norovirus infections, which suggests that antibody prevalence and titer might correlate with these phenotypes.

    METHODS:

    Plasma samples (n = 105) from Swedish blood donors that had been genotyped for secretor (FUT2) and Lewis (Le; FUT3) genotypes and phenotyped for ABO and Le blood groups were analyzed for immunoglobulin G antibody prevalence and titers to norovirus genogroup (GG) II.4.

    RESULTS:

    The results showed that nonsecretors (se4128se428) and Lea+b- individuals not only had significantly lower antibody titers than did secretors (P < .0001) and Lea-b+ individuals (P < .0002) but were also significantly more often antibody negative (P < .05). Antibody titers in secretors were not significantly different between individuals of different Le (FUT3) genotypes or different ABO phenotypes.

    CONCLUSIONS:

    Nonsecretors and Lea+b- individuals are significantly less prone to be infected with GGII noroviruses. This new information extends previous knowledge and supports the hypothesis that nonsecretors are relatively but not absolutely resistant to norovirus infections.

  • 48. Moyes, Jocelyn
    et al.
    Cohen, Cheryl
    Pretorius, Marthi
    Groome, Michelle
    von Gottberg, Anne
    Wolter, Nicole
    Walaza, Sibongile
    Haffejee, Sumayya
    Chhagan, Meera
    Naby, Fathima
    Cohen, Adam L.
    Tempia, Stefano
    Kahn, Kathleen
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Epidemiologi och global hälsa. INDEPTH network, Accra, Ghana.
    Dawood, Halima
    Venter, Marietjie
    Madhi, Shabir A.
    Epidemiology of Respiratory Syncytial Virus-Associated Acute Lower Respiratory Tract Infection Hospitalizations Among HIV-Infected and HIV-Uninfected South African Children, 2010-20112013Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 208, nr Supplement: 3, s. S217-S226Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background. There are limited data on respiratory syncytial virus (RSV) infection among children in settings with a high prevalence of human immunodeficiency virus (HIV). We studied the epidemiology of RSV-associated acute lower respiratory tract infection (ALRTI) hospitalizations among HIV-infected and HIV-uninfected children in South Africa. Methods. Children aged <5 years admitted to sentinel surveillance hospitals with physician-diagnosed neonatal sepsis or ALRTI were enrolled. Nasopharyngeal aspirates were tested by multiplex real-time polymerase chain reaction assays for RSV and other viruses. Associations between possible risk factors and severe outcomes for RSV infection among HIV-infected and uninfected children were examined. The relative risk of hospitalization in HIV-infected and HIV-uninfected children was calculated in 1 site with population denominators. Results. Of 4489 participants, 4293 (96%) were tested for RSV, of whom 1157 (27%) tested positive. With adjustment for age, HIV-infected children had a 3-5-fold increased risk of hospitalization with RSV-associated ALRTI (2010 relative risk, 5.6; [95% confidence interval (CI), 4.5-6.4]; 2011 relative risk, 3.1 [ 95% CI, 2.6-3.6]). On multivariable analysis, HIV-infected children with RSV-associated ALRTI had higher odds of death (adjusted odds ratio. 31.1; 95% CI, 5.4-179.8) and hospitalization for >5 days (adjusted odds ratio, 4.0; 95% CI, 1.5-10.6) than HIV-uninfected children. Conclusion. HIV-infected children have a higher risk of hospitalization with RSV-associated ALRTI and a poorer outcome than HIV-uninfected children. These children should be targeted for interventions aimed at preventing severe RSV disease.

  • 49. Mårtensson, Andreas
    et al.
    Ngasala, Billy
    Ursing, Johan
    Veiga, M. Isabel
    Wiklund, Lisa
    Membi, Christopher
    Montgomery, Scott M.
    Örebro universitet, Hälsoakademin.
    Premji, Zul
    Färnert, Anna
    Björkman, Anders
    Influence of consecutive-day blood sampling on polymerase chain reaction-adjusted parasitological cure rates in an antimalarial-drug trial conducted in Tanzania2007Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 195, nr 4, s. 597-601Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    We assessed the influence that consecutive-day blood sampling, compared with single-day blood sampling, had on polymerase chain reaction (PCR)-adjusted parasitological cure after stepwise genotyping of merozoite surface proteins 2 (msp2) and 1 (msp1) in 106 children in Tanzania who had uncomplicated falciparum malaria treated with either sulfadoxine-pyrimethamine or artemether-lumefantrine; 78 of these children developed recurrent parasitemia during the 42-day follow-up period. Initial msp2 genotyping identified 27 and 33 recrudescences by use of single- and consecutive-day sampling, respectively; in subsequent msp1 genotyping, 17 and 21 of these episodes, respectively, were still classified as recrudescences; these results indicate a similar sensitivity of the standard single-day PCR protocol--that is, 82% (27/33) and 81% (17/21), in both genotyping steps. Interpretation of PCR-adjusted results will significantly depend on methodology.

  • 50.
    Nayeri, Fariba
    et al.
    Linköpings universitet, Institutionen för molekylär och klinisk medicin, Infektionsmedicin. Linköpings universitet, Hälsouniversitetet.
    Nilsson, Ingela
    Department of Clinical Chemistry, County Hospital, Kalmar.
    Hagberg, Lars
    Department of Infectious Diseases, Sahlgrenska Hospital, Göteborg.
    Brudin, Lars
    Department of Clinical Physiology, County Hospital, Kalmar.
    Roberg, Magnus
    Department of Infectious Diseases, County Hospital, Norrköping, Sweden .
    Söderström, Claes
    Department of Infectious Diseases, County Hospital, Kalmar.
    Forsberg, Pia
    Linköpings universitet, Institutionen för molekylär och klinisk medicin, Infektionsmedicin. Linköpings universitet, Hälsouniversitetet.
    Hepatocyte Growth Factor Levels in Cerebrospinal Fluid: A Comparison between Acute Bacterial and Nonbacterial Meningitis2000Ingår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 181, nr 6, s. 2092-2094Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The organotrophic functions of the hepatocyte growth factor (HGF) have been the subject of several studies. In the more recent studies, this function has been reported in the brain. In the present study, we have measured the levels of HGF in cerebrospinal fluid (CSF) and sera from 78 patients divided into 6 different groups according to central nervous system (CNS) infection and control. Quantitative measurements of HGF in the CSF and serum were performed by an enzyme-linked immunosorbent assay. Elevated values of CSF HGF were found in the patients with acute bacterial/probable bacterial meningitis (P < .001), compared with nonbacterial CNS infections and facial palsy, as well as with a control group without signs of CNS involvement. The values of CSF HGF were not correlated to blood-brain-barrier disruption in the groups. These observations might indicate an intrathecal production of HGF in acute bacterial/probable bacterial meningitis.

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