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It has been well documented that cytolethal distending toxin (CDT) from  Helicobacter hepaticus  ( H. hepaticus ),  Campylobacter jejuni  ( C. jejuni ) and other Gram-negative intestinal pathogens is linked to the inflammatory bowel disease (IBD). However, the mechanisms underlying the progression of  H. hepaticus  induced colitis remains unclear. In this study, male B6.129P2- IL10 tm1Cgn  /J mice were infected by  H. hepaticus  and ΔCdtB  H. hepaticus  for 6, 12, 18, and 24 weeks. Histopathology,  H. hepaticus  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  H. hepaticus  in colon of B6.129P2- IL10 tm1cgn    / J mice, and there was no significant difference in abundance of colonic  H. hepaticus  over infection duration.  H. hepaticus  aggravated rectocele and proximal colonic inflammation, especially at 24 WPI, while ΔCdtB  H. hepaticus  could not cause significant symptom. Furthermore, mRNA levels of  Il-6 ,  Tnf-α ,  Il-1β , and  iNOS  significantly increased in the proximal colon of  H. hepaticus -infected mice compared to ΔCdtB  H. hepaticus  infected group from 12 WPI to 24 WPI. In addition, the elevated content of NO and activated  Stat3  and  Jak2  in colon were observed in  H. hepaticus  infected mice. These data demonstrated that CdtB promote colitis development in male B6.129P2- IL10 tm1Cgn  /J mice by induction of inflammatory response and activation of  Jak - Stat  signaling pathway.

frontiers in cellular and infection microbiology

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