Helicobacter pylori intragastric colonization and migration: Endoscopic manifestations and potential mechanisms

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.

Unveiling early stage autoimmune gastritis: novel endoscopic insights from two case reports

“…When H. pylori infection is absent, normal gastric mucosa features a distinctive regular arrangement of CVs (20)(21)(22). When H. pylori infects the gastric mucosa, superficial inflammation causes elongation of the gastric pits, thus rendering these venules invisible on the mucosal surface (23). In early-stage AIG, lymphocytic infiltration originates from deeper layers, allowing for the possible observation of CVs if the gastric pits remain unaffected.…”

The prospect of probiotics in -induced peptic ulcer disease: A perspective review

“…11 The colonisation of the gastric epithelium can be attributed to its ability to navigate through secretions and its predilection for areas of stomach injury. 12 It frequently infects the stomach, and approximately fifty percent of the population is asymptomatic with an H. pylori infection. This is owing to its capacity to endure short-lived pH levels below 4, although growth is inhibited at such levels; infection exclusively transpires within a restricted pH spectrum of 5.5 to 8.0.…”