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Campylobacter jejuni ‐induced transcytosis of commensal Escherichia coli across enterocytes requires plasma membrane cholesterol
Author(s) -
Kalischuk Lisa D,
Inglis G. Douglas,
Buret Andre G.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a765
Subject(s) - campylobacter jejuni , microbiology and biotechnology , enterocyte , internalization , transcytosis , chromosomal translocation , paracellular transport , biology , intestinal permeability , transcellular , lipid raft , intestinal epithelium , inflammatory bowel disease , pathogen , bacteria , endocytosis , immunology , epithelium , cell , signal transduction , small intestine , medicine , biochemistry , disease , permeability (electromagnetism) , genetics , membrane , gene
Bacterial gastroenteritis has 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 a common intestinal pathogen, Campylobacter jejuni , can induce translocation of commensal bacteria across enterocytes. Confluent, polarized enterocyte monolayers (T84) were inoculated with non‐invasive E. coli HB101 ± C. jejuni 81–176 and assayed for translocation and internalization of E. coli and epithelial permeability. Compared to the control treatment, C. jejuni induced a significant increase in E. coli translocation. This was associated with increased internalization of E. coli as determined by a gentamicin protection assay. There was no effect on epithelial permeability to a fluorescent dextran probe (3000 MW). Translocation of E. coli was prevented by treatment with the cholesterol‐disrupting drugs methyl‐â‐cyclodextrin plus lovastatin. Thus, C. jejuni may contribute to the pathogenesis of IBD by inducing translocation of non‐invasive commensal bacteria across the intestinal epithelium to the underlying mucosa via a transcellular process involving lipid‐rafts. Research supported by NSERC and the Crohn’s and Colitis Foundation of Canada.