H. pylori colonization and persistence factors
During initial infection of the stomach lumen, urease-dependent ammonia production locally raises the pH, which promotes bacterial survival and solubilizes the mucus gel to facilitate bacterial motility. Chemotaxis(driven by pH and possibly other gradients) and helical rod shape promote flagellar-based motility away from the acidic lumen to H. pylori‘s preferred niche, on and adjacent to gastric epithelial cells. SabA, BabA and other variably expressed adhesins may shift the balance to cell-associated bacteria. Inset: cell-associated bacteria alter gastric epithelial cell behavior through VacA, CagA and CagL which all have multiple cellular targets. This includes CagA and VacA dependent disruption of cell polarity that can promote iron acquisition or cell extrusion, CagA and CagL dependent induction of chemokines and/or the gastric hormone gastrin, CagL dependent inhibition of acid secretion by the H+/K+ ATPase, and affects on proliferation, apoptosis and differentiation mediated by all three effectors. As noted in the main text, in addition to CagL (depicted), CagA and CagY have also been shown to bind α5β1 integrins although the precise interaction surface remains to be determined. fla, flagella; che, chemotaxis; ure, urease; T4SS, Cag Type IV secretion system; PS, phosphatidylserine; α5β1 and αvβ5, indicated integrin subunits.