Low pH amplifies chemotaxis toward urea in Helicobacter pylori.

Helicobacter pylori infections increase the risk of noncardia gastric adenocarcinoma, and chemotaxis toward metabolites such as urea plays a key role in modulating infection. Chemotaxis studies are more insightful in strains of H. pylori that are amenable to genetic modification, such as the G27 strain. However, motility in G27 cells can be inconsistent and varies with growth conditions, raising questions about its chemotaxis abilities. Here, we quantitatively compared motility and urea chemotaxis between the G27 strain and the highly motile premouse SS1 (PMSS1) strain. We observed that G27 cells swim ∼40% slower than the PMSS1 cells, likely because the former possessed one flagellum on average, whereas the latter had multiple flagella. Despite its slow swimming, G27 exhibited a strong chemotactic response to urea with optimal output under physiological temperature (37°C). Significantly, low pH conditions amplified the urea response, and comparisons of the experiments with a mathematical model suggested that low pH increases chemoreceptor sensitivity toward the metabolite. These results are consistent with the possibility that the harsh acidic environment of the stomach enhances migration toward urea, which the cells degrade to neutralize the local pH and facilitate their survival.