Induce Colitis in Male IL-10 Mice Dependent by Cytolethal Distending Toxin B and the Activation of Jak/Stat Signaling Pathway.

It has been well documented that cytolethal distending toxin (CDT) from (), () and other Gram-negative intestinal pathogens is linked to the inflammatory bowel disease (IBD). However, the mechanisms underlying the progression of induced colitis remains unclear. In this study, male B6.129P2- /J mice were infected by and ΔCdtB for 6, 12, 18, and 24 weeks. Histopathology, colonization levels, expression of inflammatory cytokines, signaling pathways, and content of NO in proximal colon were examined. We found that Cytolethal distending toxin subunit B (CdtB) deletion had no influence on colonization ability of in colon of B6.129P2-J mice, and there was no significant difference in abundance of colonic over infection duration. aggravated rectocele and proximal colonic inflammation, especially at 24 WPI, while ΔCdtB could not cause significant symptom. Furthermore, mRNA levels of , , , and significantly increased in the proximal colon of -infected mice compared to ΔCdtB infected group from 12 WPI to 24 WPI. In addition, the elevated content of NO and activated and in colon were observed in infected mice. These data demonstrated that CdtB promote colitis development in male B6.129P2- /J mice by induction of inflammatory response and activation of - signaling pathway.