title: Rapid loss of motility of Helicobacter pylori in the gastric lumen in vivo.
abstract: The human pathogen Helicobacter pylori has infected more than half of the world's population. Nevertheless, the first step of infection, the acute colonization of the gastric mucus, is poorly understood. For successful colonization, H. pylori must retain active motility in the gastric lumen until it reaches the safety of the mucus layer. To identify the factors determining the acute colonization, we inserted bacteria into the stomach of anesthetized Mongolian gerbils. We adjusted the gastric juice to defined pH values of between 2.0 and 6.0 by using an autotitrator. Despite the fact that Helicobacter spp. are known to survive low pH values for a certain time in vitro, the length of time that H. pylori persisted under the assay conditions within the gastric juice in vivo was remarkably shorter. In the anesthetized animal we found H. pylori to be irreversibly immotile in less than 1 min at lumen pH values of 2 and 3. At pH 4 motility was lost after 2 min. However, the period of motility increased to more than 15 min at pH 6. Blocking pepsins in the gastric lumen in vivo by using pepstatin significantly increased the period of motility. It was possible to simulate the rapid in vivo immotilization in vitro by adding pepsins. We conclude that pepsin limits the persistence of H. pylori in the gastric chymus to only a few minutes by rapidly inhibiting active motility. It is therefore likely that this short period of resistance in the gastric lumen is one of the most critical phases of Helicobacter infection.
authors.affiliation: Institut für Physiologie, MA 2/149, Ruhr-Universitaet Bochum, Universitaetsstrasse 150, D-44801 Bochum, Germany. soeren.schreiber@rub.de
authors.forename: Sören
authors.initials: S
authors.lastname: Schreiber
authors.forename: Roland
authors.initials: R
authors.lastname: Bücker
authors.forename: Claudia
authors.initials: C
authors.lastname: Groll
authors.forename: Marina
authors.initials: M
authors.lastname: Azevedo-Vethacke
authors.forename: Désirée
authors.initials: D
authors.lastname: Garten
authors.forename: Peter
authors.initials: P
authors.lastname: Scheid
authors.forename: Susanne
authors.initials: S
authors.lastname: Friedrich
authors.forename: Sören
authors.initials: S
authors.lastname: Gatermann
authors.forename: Christine
authors.initials: C
authors.lastname: Josenhans
authors.forename: Sebastian
authors.initials: S
authors.lastname: Suerbaum
mesh_terms: D000818:Animals; D005753:Gastric Mucosa / Q000382:microbiology*; D005849:Gerbillinae; D016481:Helicobacter Infections / Q000382:microbiology; D016480:Helicobacter pylori / Q000254:growth & development / Q000472:pathogenicity / Q000502:physiology*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D009068:Movement; D010434:Pepsin A / Q000494:pharmacology; D010436:Pepstatins / Q000494:pharmacology; D013997:Time Factors
chemical_list: D010436:Pepstatins; D010434:Pepsin A; C031375:pepstatin
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