CsrA regulates Helicobacter pylori J99 motility and adhesion by controlling flagella formation.

Motility mediated by the flagella of Helicobacter pylori has been shown to be required for normal colonization and is thought to be important for the bacteria to move toward the gastric mucus in niches adjacent to the epithelium. Barnard et al. showed that CsrA appears to be necessary for full motility and the ability to infect mice, but its mechanism of regulation is still unclear. Motility and cell adhesion ability were determined in wild-type, csrA mutant, and revertant J99 strains. The bacterial shape and flagellar structure were evaluated by transmission electron microscopy. The expression of two major flagellins, flaA/flaB, and the alternative sigma factor rpoN (σ(54)) were determined by real-time quantitative RT-PCR and Western blot. The csrA mutant showed loss of motility and lower adhesion ability compared with the wild-type and revertant J99 strains. The csrA mutant was not flagellated. Transcription of flaA and flaB mRNA decreased to only 40% and 16%, respectively, in the csrA mutant compared with the wild-type J99 (p = .006 and <.0001, respectively), and Western blot analysis showed dramatically reduced FlaA/FlaB proteins in a csrA mutant. The disruption of csrA also decreased expression of rpoN to 48% in the csrA mutant, but the degradation rate of rpoN mRNA was not changed. These results suggest that CsrA regulates H. pylori J99 flagella formation and thereby affects bacterial motility.