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088 CAMPYLOBACTER JEJUNI INDUCES TRANSCYTOSIS OF COMMENSAL ESCHERICHIA COLI ACROSS GUT EPITHELIAL CELLS: A ROLE FOR LIPID-RAFTS LD Kalischuk1,2,3, GD Inglis3, AG Buret1,2 Campylobacter jejuni is one of the most prevalent causes of acute bacterial gastroenteritis in Canada. Bacterial intestinal infections have been implicated as a risk factor for the subsequent development of inflammatory bowel disease (IBD); however the mechanism by which this occurs is unknown. As there is compelling evidence that IBD is associated with an exaggerated immune response to commensal gut flora, we examined whether C. jejuni can induce the translocation of commensal bacteria across intestinal epithelial cells. Confluent, polarized monolayers of human colonic epithelial cells (T84) were inoculated with E. coli HB101 ± C. jejuni 81-176 and assayed for translocation and internalization of E. coli and epithelial permeability. Minimal apical to basolateral translocation of E. coli was observed in control-treated monolayers. In contrast, C. jejuni-treatment caused a significant increase in the translocation of E. coli. This was associated with increased internalization of E. coli as determined by a gentamicin protection assay and there was no effect on epithelial permeability to a fluorescent dextran probe (3000 MW). C. jejuni-mediated translocation of E. coli was prevented by pretreatment with the cholesterol-disrupting drugs methyl-beta-cyclodextrin plus lovastatin. Thus, during acute Campylobacter gastroenteritis, normally non-invasive commensal bacteria may be translocated across gut epithelial cells via a trancellular process possibly involving lipid-rafts. This increased translocation of commensal flora across the intestinal epithelium to the underlying mucosa may contribute to the pathogenesis of IBD.
1Department of Biological Sciences, 2Mucosal Inflammation Research Group, University of Calgary, Calgary; 3Agriculture and Agri-Food Canada, Lethbridge, Alberta