Immune response modulation in inflammatory bowel diseases by Helicobacter pylori infection

Figure 3 Hypothesis on correlation between concomitant infection with Helicobacter pylori and the presence of ulcerative colitis (inflammatory bowel disease), which has a pathological pattern of exacerbated T helper 2 response. The schematic shows HP-NAP being secreted into the gastric mucosa by Helicobacter pylori (H. pylori). Then, HP-NAP undergoes a process of transcytosis by endothelial cells, binding to the luminal side of the blood vessel. With this, there is an alteration in the expression of β-2-integrin, with the recruitment of neutrophils and monocytes, which carry out diapedesis. The recruited leukocytes secrete cytokines [interleukin (IL)-12 and IL-23], which promote a polarization of the circulating lymphocytes to a T helper 1 (Th1) pattern. The Th1 polarization causes a reduction in the Th2 response, this could explain the improvement of ulcerative colitis symptoms in patients infected with H. pylori. H. pylori: Helicobacter pylori; IL: Interleukin; Th: T helper; HP-NAP: Helicobacter pylori neutrophil-activating protein.