Abstract
Motility mediated by the flagella of Helicobacter pylori is important for the cells to move toward the gastric mucus in niches adjacent to the epithelium; then, H. pylori uses the adhesin SabA to interact with sialyl-Le(x) on inflammatory host cells for persistent infection. Here, we reveal the clinical association of bacterial motility, SabA expression, and pathological outcomes. Ninety-six clinical isolates were screened for bacterial motility, and the expression of SabA of each isolate was confirmed by Western blotting. H. pylori-infected patients were assessed for their bacterial density, sialyl-Le(x) expression, inflammatory scores, and clinical diseases. The mean diameter in the motility assay was 17 mm, and eight (8.3%) of the strains had impaired motility, with a diameter <5 mm. H. pylori density in cardia, the acute inflammatory score in the body locus, and the prevalence rate of gastric atrophy were increased in patients infected with higher-motility strains (p = .023, <.001, or <.001, respectively). The total inflammatory scores (both acute and chronic) and bacterial density dramatically increased in patients expressing the sialyl-Le(x) antigen and infected with higher-motility, SabA-positive H. pylori (p = .016, .01, or .005, respectively). These results suggest that the higher motility of H. pylori enhances pathological outcomes, and the SabA-sialyl-Le(x) interaction has a synergistic effect on virulence of the higher-motility strains.
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