Higher Motility Enhances Bacterial Density and Inflammatory Response in Dyspeptic Patients Infected with Helicobacter pylori

Abstract

Background 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‐Lex on inflammatory host cells for persistent infection. Here, we reveal the clinical association of bacterial motility, SabA expression, and pathological outcomes. Methods 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‐Lex expression, inflammatory scores, and clinical diseases. Results 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‐Lex antigen and infected with higher‐motility, SabA‐positive H. pylori (p = .016, .01, or .005, respectively). Conclusion These results suggest that the higher motility of H. pylori enhances pathological outcomes, and the SabA–sialyl‐Lex interaction has a synergistic effect on virulence of the higher‐motility strains.

The complex interplay among bacterial motility and virulence factors in different Escherichia coli infections

“…In E. coli and Pseudomonas aeruginosa, flagellin and/or the distally located flagellar cap protein have been reported to function as adhesins [25]. The combination of virulence factor expression and higher motility of H. pylori leads to synergistic effects on gastric pathology [8]. This study, showing a greater prevalence of afa and ompT genes in the lower-motility E. coli isolates, suggests that more bacterial virulence traits may be necessary for the development of clinical E. coli infections by lower-motility strains.…”

“…In the pathogenesis of SBP, bacterial translocation from the intestine into the mesenteric lymph nodes, followed by bacteremia and ascitic fluid colonization due to impaired local and systemic immunity, are considered to be two important steps [21,22]. In our previous study, higher H. pylori motility was associated with increased H. pylori density and inflammation severity, and the prevalence rate of gastric atrophy was increased in dyspeptic patients infected with higher-motility strains [8]. We speculate that higher E. coli motility might increase the bacterial density on, and enhance the inflammatory response of, intestinal enterocytes, and contribute to the translocation of E. coli from the intestinal lumen and development of SBP in cirrhotic patients.…”

“…The motility assay has been described previously [8]. In brief, several colonies were applied to one spot in the motility agar plate containing LB broth (Difco) and 0.3 % Bacto agar.…”

“…Flagellar motility has been shown to be essential for the pathogenesis of several bacteria, including Proteus mirabilis [2,3], Salmonella species [4,5], Helicobacter pylori [6], and enteropathogenic E. coli [7]. Our previous study demonstrated that the H. pylori density in the cardia, the acute inflammatory score in the body locus, and the prevalence rate of gastric atrophy were increased in patients infected with more motile H. pylori [8].…”

Helicobacter pylori—Associated Dyspepsia in Paediatrics

“…As already mentioned in this chapter (see section 1.2.1 of this chapter) motility is a long known virulence-related trait [46], with lower-motility associated reduced inflammation levels [47] and with non-motile strains unable to establish a robust infection [42,45,46]. Moreover, it was more recently shown that higher motility enhances H. pylori density and inflammatory response in dyspeptic patients [130].…”