Helicobacter bilis Contributes to the Occurrence of Inflammatory Bowel Disease by Inducing Host Immune Disorders

Figure 1

H. bilis promotes IBD through inducing aberrant immune responses in the host. (a) H. bilis colonization could increase the expression of numerous mucosal genes (e.g., Fut2, B3galt5, Ceacam12, Cyp4b1, and Ugt8a), which could lead to increased protein glycosylation and dysregulation of detoxification. (b) H. bilis colonization could increase the expression of genes associated with T cell activation and chemotaxis (e.g., Cd28, Ccl8, Ccr5, and Itgb2). (c) H. bilis affects bacterial quorum sensing by secreted autoinducer factors in the human intestine, resulting in structural changes of the gut microbiota. (d) H. bilis releases a specific virulence factor HBgGT to induce oxidative stress response cascades in colon epithelial cells. (e) H. bilis colonization could increase the expression of IL-1 family secreted by macrophages, and these cytokines are associated with proinflammatory signaling. H. bilis: Helicobacter bilis; ROS: reactive oxygen species; HBgGT: H. bilis gamma-glutamyl transpeptidase.