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Barrier dysfunction and bacterial uptake in the follicle-associated epithelium of ileal Crohns disease
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Kirurgi. Linköpings universitet, Hälsouniversitetet.
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Kirurgi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Centrum för kirurgi, ortopedi och cancervård, Kirurgiska kliniken US.
2012 (engelsk)Inngår i: Annals of the New York Academy of Sciences, ISSN 0077-8923, E-ISSN 1749-6632, Vol. 1258, nr 1, s. 125-134Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

The ability to control uptake across the mucosa and protect from harmful substances in the gut lumen is defined as intestinal barrier function. The etiology of Crohns disease is unknown, but genetic, environmental, and immunological factors all contribute. The frontline between these factors lies in the intestinal barrier. The most important inflammation-driving environmental factor in Crohns disease is the microbiota, where Esherichia coli strains have been assigned a key role. The first observable signs of Crohns disease are small aphtoid ulcers over Peyers patches and lymphoid follicles. The overlaying follicle-associated epithelium (FAE) is specialized for luminal sampling and is an entry site for antigens and bacteria. We have demonstrated increased E. coli uptake across the FAE in Crohns disease, which may initiate inflammation. This short review will discuss barrier dysfunction and bacteria in the context of ileal Crohns disease, and how the FAE might be the site of initial inflammation.

sted, utgiver, år, opplag, sider
2012. Vol. 1258, nr 1, s. 125-134
Emneord [en]
adherent invasive E. coli; etiology; inflammatory bowel disease; pathogens; Peyer's patches
HSV kategori
Identifikatorer
URN: urn:nbn:se:liu:diva-80250DOI: 10.1111/j.1749-6632.2012.06502.xOAI: oai:DiVA.org:liu-80250DiVA, id: diva2:546327
Tilgjengelig fra: 2012-08-23 Laget: 2012-08-23 Sist oppdatert: 2017-12-07

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