Motility as a factor in the colonisation of gnotobiotic piglets by Helicobacter pylori

Abstract

Summary. Non-motile variants of Helicobacterpylori (strain 26695) occurred with a frequency of 1.6 (SD 0.4) x lo-* variants/cell/division cycle, and reversion to the motile form occurred with a frequency of < lo-' variants/cell/division cycle. The two forms remained > 90 YO pure for up to 50 cell divisions and differed only in the presence or absence of motility and flagella. Bacteria were recovered from nine of 10 gnotobiotic piglets inoculated orally with motile H. pylori, but from only two of eight inoculated with the non-motile variant. The motile form survived for 21 days in infected piglets, but the non-motile variant survived for only 6 days. Bacteria recovered from piglets inoculated with the non-motile variant were non-motile. These data support the hypothesis that motility is a colonisation factor for H . pylori.

Helicobacter pylori Urease Binds to Class II MHC on Gastric Epithelial Cells and Induces Their Apoptosis

“…The observation that urease binds to class II MHC on gastric epithelial cells may help explain why urease-negative mutants of H. pylori failed to colonize in an animal model of infection even under hypochlorhydric conditions (6). In other studies with ureasenegative mutants, it was speculated that the failure to colonize was due to a requirement of the enzymatic activity to provide a more hospitable environment for H. pylori to grow (5,36).…”

“…Isogenic mutant H. pylori strains showed that urease is essential for colonization because the mutant bacteria were unable to colonize gnotobiotic pigs (5). However, the urease-negative H. pylori strains also failed to colonize under hypochlorhydric conditions (6), which suggested a role for urease in colonization beyond its ability to neutralize the gastric acidity.…”

Characterization of flagella genes of Agrobacterium tumefaciens, and the effect of a bald strain on virulence

“…typhimurium (Jones et al, 1992;Khoramianfalsafi et al, 1990), Helicobacter pylori (Eaton et al, 1992), and Bacillus thuringiensis (Zhang et al, 1993). With regard to plant pathogens, correlations between chemotaxis, motility, and virulence were found for Xanthomonas campestris pv.…”

Augmentation of Helicobacter pylori urease activity by its specific IgG antibody: implications for bacterial colonization enhancement

“…Also, the enhancement of the urease activity on the surface of H. pylori by binding with pre-administrated S3 MAb secreted from gastric mucosa may augment the ability to colonize onto the gastric mucosa through association with the class II MHC molecules expressed on the gastric epithelial cells (10,11). Indeed, there are a number of reports showing that H. pylori urease expressing outside of the bacteria seems to be a critical factor for adhering to the gastric mucosa and urease-negative H. pylori strains as well as the urease mutants failed to colonize the gastric compartment (6,8).…”