The Role of Microcin B17-Producing Escherichia Coli, Isolated from Patients with Inflammatory Bowel Disease on Rat Intestine

Background: Inflammatory Bowel Disease (IBD) is a chronic gastrointestinal disease, Crohn’s disease (CD) and ulcerative colitis (UC) are two distinct kinds of IBD. Recent researches have linked between Escherichia coli which produce the toxin microcin B17 (E. coli/+mB17) and the development of inflammatory bowel disease (IBD). Objective: This study aimed to demonstrate the relationship between these E. coli isolates and the emergence of IBD in an experimental animal models. Materials and Methods: Twenty female rats, five-weeks-old were divided in to four groups; first group, were orally given E. coli/+mB17 isolated from crohn’s patients stool, the second group rats were orally given E. coli/+mB17 isolated from patients stool with ulcerative colitis, in the third group were orally given E. coli non-producing microcin B17 (E. coli/-mB17) isolated from patients stool with IBD, and the last group received normal saline orally, as control. After fifteen weeks of administration, Blood was drawn for serological tests which include interlukin-10 (IL-10) and tumor necrosis factor-α (TNF-α) and the rats sacrificed for evaluation of histological changes in their intestine. Results: All groups that were administrated bacteria, whether they were toxin producer or not, showed a decrease in their weights with a reduction of appetite. Serological changes observed included an increase in IL-10 level and an increase in TNF-α level in their sera. Regarding the histological examination, there were noticeable histological changes in the large intestines of all rats given bacterial suspension but not in small intestine. Conclusion: All E.coli isolates which were isolated from IBD patients stool (whether it was microcin B17 producing or not) were able to induce inflammatory responses and histological changes in the intestines of rats . Accordingly, other virulence factors (in addition to Microcin B17) may play role in the pathogenesis of IBD.