Affiliation:
1. Department of Microbiology1 and
2. First Department of Internal Medicine,2 Yamaguchi University School of Medicine, Ube, Yamaguchi 755-8505, and
3. Department of Environmental Science, Yamaguchi Prefectural University, Yamaguchi 753-0011,3 Japan
Abstract
ABSTRACT
Helicobacter pylori
exhibits chemotactic responses to urea, flurofamide, acetohydroxamic acid, and sodium bicarbonate. In buffer, the chemotactic activities of a urease-positive strain were higher than those of the isogenic urease-negative strain. Moreover, the chemotactic activities of the urease-positive strain were increased in a viscous solution containing 3% polyvinylpyrrolidone, whereas those of the urease-negative mutant were not. These results are in accordance with the fact that the mutant strain did not show swarming in motility agar regardless of having flagella. Incubation of the wild-type strain with flurofamide resulted in partial inhibition of the chemotactic activities in the viscous solution. In addition, incubation with acetohydroxamic acid, a low-molecular-weight, diffusible urease inhibitor, resulted in complete loss of chemotactic activity in the viscous solution. The inhibition of the chemotactic activity by urease inhibitors paralleled the inhibition of urease. The chemotactic activity of
H. pylori
was also inhibited by the proton carrier carbonyl cyanide
m
-chlorophenylhydrazone, showing that
H. pylori
utilizes proton motive force for motility. These results indicate that cytoplasmic urease plays an important role in the chemotactic motility of
H. pylori
under a condition that mimics the ecological niche of the bacterium, the gastric mucous layer.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
93 articles.
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