Abstract
Background: Phylogroup B2 Escherichia coli have been associated with ulcerative colitis (UC). In this study, we aimed to compare colonization with the UC-associated E. coli p19A in different mice strains, to investigate the role of alpha hemolysin in a UC mouse model. Methods: In this study, Sigirr −/− and C57BL/6 mice were chosen, and UC was induced by adding dextran sulfate sodium (DSS) to the drinking water. The mice were pre-treated with ciprofloxacin. p19A expressing luminescence and GFP, alpha-hemolysin knock out p19A-ΔhlyI II, and non-pathogenic lab E. coli DH10B were cultured in LB broth, and orally gavaged into the mice. Colonization with p19A WT was visualized using an in vivo imaging system. Results: p19A WT colonized the colon, ileum, Peyer’s patches, liver, and spleen of infected C57BL/6 and Sigirr −/− mice. A total of 99% of the p19A WT infected C57BL/6 mice and 29% of the p19A WT infected Sigirr −/− mice survived to the 4th post infection day. Conclusion: UC-associated E. coli p19A WT colonized the intestines of DSS-treated mice and caused extra-intestinal infection. Hemolysin is an important factor in this pathogenesis, since isogenic hemolysin mutants did not cause the same inflammation.
Highlights
Inflammatory bowel diseases (IBD) can be divided into ulcerative colitis (UC) and Crohn’s disease (CD)
The second and fourth trial was performed to discover the pathogenesis of p19A WT and p19A ∆hlyI, II colonization in the dextran sulfate sodium (DSS) treated C57BL/6 mice
Our results indicate that DSS treated Sigirr −/− mice, which are deficient in SIGIRR/in interleukin-1 receptor, serve as a good model for CD, where inflammation/infection occurs in the small intestine and Peyer’s patches, in comparison to the other IBD in vivo model, where inflammation occurs only in the colon
Summary
Inflammatory bowel diseases (IBD) can be divided into ulcerative colitis (UC) and Crohn’s disease (CD). The etiology of IBD is unknown, but immunological investigations of animal models have shown that intestinal inflammation is derived from changes in the intestinal microbiota [2], triggering an abnormal immune response [3]. These abnormal immune responses to intestinal microbiota changes in IBD cause activation of innate immune receptors such as Toll-like receptors (TLRs), which leads to upregulation of antimicrobial factors, and secretion of cytokines and chemokines [4]. We aimed to compare colonization with the UC-associated E. coli p19A in different mice strains, to investigate the role of alpha hemolysin in a UC mouse model. Conclusion: UC-associated E. coli p19A WT colonized the intestines of DSS-treated mice and caused extra-intestinal infection. Hemolysin is an important factor in this pathogenesis, since isogenic hemolysin mutants did not cause the same inflammation
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