Enteropathogenic e.coli sustains iodoacetamide-induced ulcerative colitis-like colitis in rats: modulation of IL-1β, IL-6, TNF-α, COX-2, and apoptosisi

• Published in: Journal of biological regulators and homeostatic agents Vol. 26; no. 3; p. 515
• Main Authors: Abdallah Hajj Hussein, I, Freund, J N, Reimund, J M, Shams, A, Yamine, M, Leone, A, Jurjus, A R
• Format: Journal Article
• Language: English; French
• Published: Italy 01.07.2012
• Subjects: Alkylating Agents - adverse effects; Alkylating Agents - pharmacology; Animals; Apoptosis - drug effects; bcl-2-Associated X Protein - biosynthesis; Colitis, Ulcerative - chemically induced; Colitis, Ulcerative - metabolism; Colitis, Ulcerative - microbiology; Colitis, Ulcerative - pathology; Colon - metabolism; Colon - microbiology; Colon - pathology; Cyclooxygenase 2 - biosynthesis; Enteropathogenic Escherichia coli; Escherichia coli Infections - chemically induced; Escherichia coli Infections - metabolism; Escherichia coli Infections - microbiology; Escherichia coli Infections - pathology; Gene Expression Regulation - drug effects; Interleukin-1beta - biosynthesis; Interleukin-6 - biosynthesis; Intestinal Mucosa - metabolism; Intestinal Mucosa - microbiology; Intestinal Mucosa - pathology; Iodoacetamide - adverse effects; Iodoacetamide - pharmacology; Male; Proto-Oncogene Proteins c-bcl-2 - biosynthesis; Rats; Rats, Sprague-Dawley; Tumor Necrosis Factor-alpha - biosynthesis
• ISSN: 0393-974X

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.