Immune response modulation in inflammatory bowel diseases by Helicobacter pylori infection

Abstract

Many studies point to an association between Helicobacter pylori (H. pylori) infection and inflammatory bowel diseases (IBD). Although controversial, this association indicates that the presence of the bacterium somehow affects the course of IBD. It appears that H. pylori infection influences IBD through changes in the diversity of the gut microbiota, and hence in local chemical characteristics, and alteration in the pattern of gut immune response. The gut immune response appears to be modulated by H. pylori infection towards a less aggressive inflammatory response and the establishment of a targeted response to tissue repair. Therefore, a T helper 2 (Th2)/macrophage M2 response is stimulated, while the Th1/macrophage M1 response is suppressed. The immunomodulation appears to be associated with intrinsic factors of the bacteria, such as virulence factors - such oncogenic protein cytotoxin-associated antigen A, proteins such H. pylori neutrophil-activating protein, but also with microenvironmental changes that favor permanence of H. pylori in the stomach. These changes include the increase of gastric mucosal pH by urease activity, and suppression of the stomach immune response promoted by evasion mechanisms of the bacterium. Furthermore, there is a causal relationship between H. pylori infection and components of the innate immunity such as the NLR family pyrin domain containing 3 inflammasome that directs IBD toward a better prognosis.

Keywords: Cytotoxin-associated antigen A oncoprotein; Gut microbiota; Helicobacter pylori; Helicobacter pylori neutrophil-activating protein; Immunological modulation; Inflammatory bowel disease; NLR family pyrin domain containing 3 inflammasome

Core Tip:Helicobacter pylori (H. pylori) infection seems to modulate the immune response triggered by inflammatory bowel disease in a way that makes it less aggressive. The virulence factors of H. pylori, as well as the mechanisms that allow it to remain in the stomach environment, appear to change the intestinal microenvironment and modulate the local immune response, contributing to a disease with milder symptoms and less tissue damage.