Although the exact protective mechanisms of H. pylori against IBD remain to be fully elucidated, evidence from murine models highlights regulated Th17/Treg cell responses, modulation of NLRP12 expression, and decreased levels of pro‐inflammatory mediators such as COX‐2, TGF‐β, TNF‐α, and tissue transglutaminase (t‐TG) as plausible explanations. This evidence concerns the gene TNF and inflammatory bowel disease.