Helicobacter pylori Uses the TlpB Receptor To Sense Sites of Gastric Injury.

is a pathogen that chronically colonizes the stomachs of approximately half of the world's population and contributes to the development of gastric inflammation. We demonstrated previously that uses motility to preferentially colonize injury sites in the mouse stomach. However, the chemoreceptor responsible for sensing gastric injury has not yet been identified. In this study, we utilized murine gastric organoids (gastroids) and mutant strains to investigate the components necessary for chemotaxis. High-intensity 730-nm light (two-photon photodamage) was used to cause single-cell damage in gastroids, and repair of the damage was monitored over time; complete repair occurred within ∼10 min in uninfected gastroids. Wild-type accumulated at the damage site after gastric damage induction. In contrast, mutants lacking motility (Δ) or chemotaxis (Δ) did not accumulate at the injury site. Using mutants lacking individual chemoreceptors, we found that only TlpB was required for accumulation, while TlpA, TlpC, and TlpD were dispensable. All strains that were able to accumulate at the damage site limited repair. When urea (an identified chemoattractant sensed by TlpB) was microinjected into the gastroid lumen, it prevented the accumulation of at damage sites. Overall, our findings demonstrate that colonizes and limits repair at damage sites via chemotactic motility that requires the TlpB chemoreceptor to sense signals generated by gastric epithelial cells.