Rayment, N.; Mylonaki, M.; Hudspith, B.; Brostoff, J.; Rampton, D.S.
April 2003
Gut;Apr2003 Supplement 1, Vol. 52, pA13
Academic Journal
Background: Gut bacterial flora are thought to play a pathogenic role in IBD. We and others have previously reported the presence of E coli, but not other commensals, in the lamina propria of patients with active IBD (Gut 2002;50(Suppl II) A29; Scand J Gastroenterol 2002;37:1034-41). We have now investigated the possibility that these organisms may contribute to the pathogenesis of IBD by interaction with lamina proprial macrophages and dendritic cells. Methods: Snap frozen rectal biopsies were taken at routine colonoscopy from patients with ulcerative colitis (UC, n = 35), Crohn's (CD, n = 6), and controls with normal colorectal mucosa (n = 25). Fluorescent in situ hybridisation was used to identify E coli, bifidobacteria, lactobacillus, and bacteroides using RNA probes. Cellular coIocalisation of bacteria was sought immunohistochemically using the phenotypic markers CD68 (macrophages) and CD1a (dendritic cells). Results: In controls and patients with inactive IBD, all four bacterial species were confined to the mucosal surface. However, individual organisms and clusters of E coli (but not other species) were seen also in the lamina propria of 7/9 patients with active UC and 4/6 those with active CD (p < 0.0004 from controls and inactive IBD). In patients with active IBD, E coli were found adjacent to (n = 7) and/or internalised by CD68+ macrophages (n = 4). E coli were not co-located with CDla+ dendritic cells in any patients (p < 0.00006 from macrophages). Conclusion: Their close apposition to, and in some cases internalisation within lamina proprial macrophages in patients with active IBD suggests that E coli could contribute to the pathogenesis of the disease.


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