Helicobacter pylori strains vary cell shape and flagellum number to maintain robust motility in viscous environments

Abstract

Summary The helical shape of the human stomach pathogen Helicobacter pylori has been suggested to provide mechanical advantage for penetrating the viscous stomach mucus layer. Using single-cell tracking and quantitative morphology analysis we document marked variation in cell body helical parameters and flagellum number among H. pylori strains leading to distinct and broad speed distributions in broth and viscous gastric mucin media. These distributions reflect both temporal variation in swimming speed and morphologic variation within the population. Isogenic mutants with straight-rod morphology showed 7–21% reduction in speed and a lower fraction of motile bacteria. Mutational perturbation of flagellum number revealed a 19% increase in speed with 4 vs. 3 median flagellum number. Resistive force theory modeling incorporating variation of both cell shape and flagellum number predicts qualitative speed differences of 10–30% among strains. However, quantitative comparisons suggest RFT underestimates the influence of cell body shape on speed for helical shaped bacteria.

Staying in Shape: the Impact of Cell Shape on Bacterial Survival in Diverse Environments

“…While initial studies suggested that like B. burgdorferi, H. pylori cell shape mutants showed swimming behavior similar to that of the wild type in methylcellulose viscous solutions (19), single-cell tracking of mul-tiple H. pylori strains revealed large temporal fluctuations in the speed of individual bacteria that may have confounded prior studies (65). Analysis of 50 to 100 cells per genotype revealed contributions of both helical shape and increased flagellar number to swimming speed in viscous gastric mucin solutions, in addition to an enhanced ability to escape from a mucin gel (65). Further work on motility specifically at physiologic concentrations of gastric and intestinal mucins, combined with exploration of the localization of helical versus nonhelical mutants within the infected host, will be needed to definitively establish the mechanism(s) by which nonhelical mutants of H. pylori and C. jejuni fail to robustly colonize their hosts.…”

“…However, the localized production of urease by H. pylori actually changes the viscoelastic properties of the surrounding mucus from a gel-like state to a viscous solution, thus challenging the corkscrew model (61). While initial studies suggested that like B. burgdorferi, H. pylori cell shape mutants showed swimming behavior similar to that of the wild type in methylcellulose viscous solutions (19), single-cell tracking of mul-tiple H. pylori strains revealed large temporal fluctuations in the speed of individual bacteria that may have confounded prior studies (65). Analysis of 50 to 100 cells per genotype revealed contributions of both helical shape and increased flagellar number to swimming speed in viscous gastric mucin solutions, in addition to an enhanced ability to escape from a mucin gel (65).…”

“…Interestingly, despite having more flagella, these lophotrichous P. putida mutants are unable to spread on 0.4% motility agar plates. In contrast, a mutation of a small RNA gene that leads to a larger median number of polar flagella in H. pylori leads to increased swimming speeds (65).…”

Bacteriological Investigation of Helicobacter pylori Infections in Patients with Gastric and Duodenal Ulcer

“…Thus, during infections, as well as the transmission by the nasogastric tube, H. pylori entered a stomach without acid, allowing the bacterium to bury into the mucous layer before normal gastric acidity was reestablished. In most cases of chronic H. pylori gastritis, there is no information of any symptomatic episode (Martínez et al, 2016).…”

Antibiotic Sensitivity to Helicobacter pylori Growth

“…Cultures are incubated under microaerobic conditions (85% N2, 10% CO 2 , 5% O 2 ) at 35 to 37ºC for at least 7 d before discarding cultures as negative. Morphological characteristics and positive catalase, oxidase, and urease reactions are used for identification of H. pylori (Martínez et al, 2016).…”