Motility and Chemotaxis Mediate the Preferential Colonization of Gastric Injury Sites by Helicobacter pylori

Aihara E, Closson C, Matthis AL, Schumacher MA, Engevik AC, Zavros Y, Ottemann KM, & Montrose MH. PLos pathogens. (2014) 10, e1004275.

Speaker: Shiau-Ting Yang (楊曉婷)                             Time: 14:00~15:00, Dec. 9, 2015

Commentator: Dr. Ching-Hao Teng (鄧景浩老師)      Place: Room 601

Abstract:

Helicobacter pylori (H. pylori) is a helical shaped, highly motile, microaerophilic, gram-negative bacterium, specialized in the colonization of the human stomach. H. pylori commonly infects approximately 50% of the world’s population and promotes gastritis, gastric ulceration, and gastric cancer ^[1]. A crucial step in the pathogenesis of H. pylori infection is when the bacterium first interacts with gastric tissue, however the events has been only limited investigation in vivo. Inoculation with 10⁶ H. pylori (wild-type Sydney Strain 1, SS1) significantly delayed healing of acetic-acid induced ulcers at Day 1, 7 and 30 post-inoculation, and wild-type SS1 preferentially accumulated at the ulcerated area compared to intact area in the same animal gastric tissue at all time points. To determine whether H. pylori can sense and migrate to the ulcerated area using chemotaxis and motility, the authors analyzed isogenic H. pylori mutants defective in chemotaxis (∆cheY) or motility (∆motB). Two-photon microscopy was used to induce gastric epithelial microlesions in anesthetized mice, and accumulation of fluorescently labeled H. pylori at damage sites in the short term time frame was evaluated. Within minutes, H. pylori SS1 preferentially accumulated at the damage sites and inhibited gastric epithelial restitution. H. pylori ∆cheY modestly accumulated at the gastric epithelial surface and inhibited restitution, but did not preferentially accumulate at the sites of damage. H. pylori ∆motB neither accumulated at the gastric surface nor inhibited restitution. The authors conclude that bacterial chemosensing and motility rapidly detect and navigate towards the ulcerated area which serve as preferential colonization sites, and thereby biases these tissue towards sustained gastric damage.

References:

1.     Marshall BJ, Warren JR. (1984) Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet (London, England). 1, 1311-1315.