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Monitoring of Protein Biomarkers of Inflammation in Human Traumatic Brain Injury Using Microdialysis and Proximity Extension Assay Technology in Neurointensive Care
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Enblad: Neurosurgery.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Molecular tools.ORCID iD: 0000-0003-2103-4253
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience. Uppsala Univ, Dept Neurosci, Sect Neurosurg, Uppsala, Sweden. (Enblad:neurokirurgi)
Uppsala University, Disciplinary Domain of Humanities and Social Sciences, Faculty of Social Sciences, Department of Statistics. Uppsala Univ, Dept Stat, Uppsala, Sweden;Univ Edinburgh, Sch Math, Edinburgh, Midlothian, Scotland;Univ Edinburgh, Maxwell Inst Math Sci, Edinburgh, Midlothian, Scotland.
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2019 (English)In: Journal of Neurotrauma, ISSN 0897-7151, E-ISSN 1557-9042, Vol. 36, no 20, p. 2872-2885Article in journal (Refereed) Published
Abstract [en]

Traumatic brain injury (TBI) is followed by secondary injury mechanisms strongly involving neuroinflammation. To monitor the complex inflammatory cascade in human TBI, we used cerebral microdialysis (MD) and multiplex proximity extension assay (PEA) technology and simultaneously measured levels of 92 protein biomarkers of inflammation in MD samples every three hours for five days in 10 patients with severe TBI under neurointensive care. One mu L MD samples were incubated with paired oligonucleotide-conjugated antibodies binding to each protein, allowing quantification by real-time quantitative polymerase chain reaction. Sixty-nine proteins were suitable for statistical analysis. We found five different patterns with either early (<48 h; e.g., CCL20, IL6, LIF, CCL3), mid (48-96 h; e.g., CCL19, CXCL5, CXCL10, MMP1), late (>96 h; e.g., CD40, MCP2, MCP3), biphasic peaks (e.g., CXCL1, CXCL5, IL8) or stable (e.g., CCL4, DNER, VEGFA)/low trends. High protein levels were observed for e.g., CXCL1, CXCL10, MCP1, MCP2, IL8, while e.g., CCL28 and MCP4 were detected at low levels. Several proteins (CCL8, -19, -20, -23, CXCL1, -5, -6, -9, -11, CST5, DNER, Flt3L, and SIRT2) have not been studied previously in human TBI. Cross-correlation analysis revealed that LIF and CXCL5 may play a central role in the inflammatory cascade. This study provides a unique data set with individual temporal trends for potential inflammatory biomarkers in patients with TBI. We conclude that the combination of MD and PEA is a powerful tool to map the complex inflammatory cascade in the injured human brain. The technique offers new possibilities of protein profiling of complex secondary injury pathways.

Place, publisher, year, edition, pages
MARY ANN LIEBERT, INC , 2019. Vol. 36, no 20, p. 2872-2885
Keywords [en]
biomarkers, inflammation, microdialysis, molecular tools, neurointensive care, proteomics, traumatic brain injury
National Category
Neurology
Identifiers
URN: urn:nbn:se:uu:diva-396069DOI: 10.1089/neu.2018.6320ISI: 000472621900001PubMedID: 31017044OAI: oai:DiVA.org:uu-396069DiVA, id: diva2:1366697
Funder
Swedish Research CouncilVinnovaAvailable from: 2019-10-30 Created: 2019-10-30 Last updated: 2019-10-30Bibliographically approved

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Dyhrfort, PhilipShen, QiujinClausen, FredrikEriksson, MånsEnblad, PerKamali-Moghaddam, MasoodLewén, AndersHillered, Lars
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