title: Enteropathogenic e.coli sustains iodoacetamide-induced ulcerative colitis-like colitis in rats: modulation of IL-1β, IL-6, TNF-α, COX-2, and apoptosisi.
abstract: Pathogenic or non-pathogenic bacteria from flora may play a key role in inflammatory bowel disease (IBD) pathogenesis. However, a specific infectious agent causing IBD has not been identified. This study assessed the impact of enteropathogenic E. coli (EPEC) on the modulation of IL-1beta, IL-6, TNF- alpha, COX-2, BAX and Bcl-2 expression, in sustaining inflammation of a rat colitis model. Two hundred male Sprague-Dawley rats (4 groups) were inoculated weekly or bi-weekly for 70 days, with 1 percent methylcellulose (MC), (b) 6 percent iodoacetamide (IA) in 1 percent MC, (c) 4x108 CFU of EPEC, and (d) IA+EPEC. After a month, treatment was stopped in half of the animals in each group. IL-1beta, IL-6, TNF-alpha, COX-2, BAX and Bcl-2 expression were measured in colonic mucosa scrapings. IL-1beta, IL-6, TNF-alpha, and COX-2 were significantly increased in colonic mucosa of the IA+EPEC group and to a lesser but significant level in the IA group compared to controls, or EPEC alone, both in continued and discontinued treatment groups. Additionally, the BAX/Bcl-2 ratio decreased, indicating less apoptosis in the IA+EPEC group which exhibited more necrosis. These effects increased with experiment duration. This work provides new arguments favouring the role of bacteria in IBD pathogenesis.
authors.affiliation: Department of Anatomy, American University Beirut, Beirut, Lebanon.
authors.forename: I
authors.initials: I
authors.lastname: Abdallah Hajj Hussein
authors.forename: J N
authors.initials: JN
authors.lastname: Freund
authors.forename: J M
authors.initials: JM
authors.lastname: Reimund
authors.forename: A
authors.initials: A
authors.lastname: Shams
authors.forename: M
authors.initials: M
authors.lastname: Yamine
authors.forename: A
authors.initials: A
authors.lastname: Leone
authors.forename: A R
authors.initials: AR
authors.lastname: Jurjus
mesh_terms: D000477:Alkylating Agents / Q000009:adverse effects* / Q000494:pharmacology; D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D003093:Colitis, Ulcerative / Q000139:chemically induced / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D003106:Colon / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D051546:Cyclooxygenase 2 / Q000096:biosynthesis*; D054308:Enteropathogenic Escherichia coli; D004927:Escherichia coli Infections / Q000139:chemically induced / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D005786:Gene Expression Regulation / Q000187:drug effects; D053583:Interleukin-1beta / Q000096:biosynthesis*; D015850:Interleukin-6 / Q000096:biosynthesis*; D007413:Intestinal Mucosa / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D007460:Iodoacetamide / Q000009:adverse effects* / Q000494:pharmacology; D008297:Male; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*; D051028:bcl-2-Associated X Protein / Q000096:biosynthesis
chemical_list: D000477:Alkylating Agents; C494828:Bax protein, rat; D053583:Interleukin-1beta; D015850:Interleukin-6; D019253:Proto-Oncogene Proteins c-bcl-2; D014409:Tumor Necrosis Factor-alpha; D051028:bcl-2-Associated X Protein; D051546:Cyclooxygenase 2; C489691:Ptgs2 protein, rat; D007460:Iodoacetamide