Molecular and Mucosal Immune Mechanisms in Infectious Gastritis and Gastroenteritis
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Abstract
Gastritis and gastroenteritis arise from pathogens whose virulence programmes interact with epithelial barriers and mucosal immunity through distinct mechanisms. This narrative review synthesizes selected evidence on Helicobacter pylori gastritis and gastroenteritis associated with norovirus and enterotoxigenic Escherichia coli (ETEC), while separately examining intestinal Candida albicans colonization and invasive disease in susceptible hosts. H. pylori uses urease, motility, adhesins, and a type IV secretion system to persist in the stomach; the effector CagA and the toxin VacA perturb epithelial integrity and inflammatory signalling. Norovirus attachment is influenced by histo-blood-group antigens and infection disrupts small-intestinal absorptive function, whereas viral variation limits durable protection. ETEC colonization factors enable mucosal adherence, and heat-labile and heat-stable enterotoxins raise cyclic AMP and cyclic GMP, respectively, producing CFTR-mediated secretory diarrhoea without substantial invasion. C. albicans is normally a gastrointestinal commensal; intestinal overgrowth or stool detection must not be equated with gastroenteritis. In profoundly susceptible hosts, yeast-to-hypha transition, candidalysin, adhesins, secreted aspartyl proteases, and biofilm formation may facilitate mucosal invasion, countered principally by epithelial sensing, Dectin-1/CARD9 signalling, neutrophils, and Th17 immunity. Because this is a narrative synthesis, conclusions depend on the scope and quality of the selected literature. Precise distinction among colonization, dysbiosis, mucosal invasion, and disseminated infection is essential for clinically meaningful interpretation.
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References
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