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H. pylori infection leads to gastric inflammation, characterised histologically by surface epithelial degeneration and infiltration of the gastric mucosa by acute and chronic inflammatory cells. H. pylori adherence, the production of a vacuolating cytotoxin and bacterial enzymes all contribute to epithelial damage. Recruitment and activation of immune cells in the underlying mucosa involves H. pylori chemotaxins, epithelial-derived chemotactic peptides (chemokines) such as IL-8 and GRO-alpha, and pro-inflammatory cytokines liberated by mononuclear phagocytes (TNF alpha, IL-1 and IL-6) as part of non-specific immunity. Antigen-specific cellular immunity results in a predominant Th1 lymphocyte response with an increase in IFN-gamma secreting T-helper cells, whilst humoral responses lead to the production of anti-H. pylori antibodies and complement activation. The complex network of cytokines implicated in these inflammatory responses include counter-regulatory elements such as IL-10 which may serve to damp down inflammation. Molecular mimicry of host structures by H. pylori, with the generation of specific immunity directed against self-antigens may also contribute to host injury. Progress in molecular biology has revealed considerable genomic diversity amongst H. pylori strains, with cag+ bacteria being associated with increased chemokine and cytokine responses and more severe degrees of gastric inflammation. Strain hetereogeneity may contribute towards the wide spectrum of disease manifestations encountered in clinical practice.
Bodger et al. (Thu,) studied this question.