Chemotaxis of Helicobacter pylori: a urease-independent response

Helicobacter pylori has adapted to a very specialized niche; namely, the highly acidic, viscous, and somewhat anaerobic gastric mucus of humans. The enzyme urease is essential for colonization of the stomach, as it provides protection against gastric acidity. A spiral morphology as well as sheathed flagella have been claimed to give the bacteria an advantage in colonizing mucus. Wild type strain of H. pylori and its isogenic urease-negative mutant showed a chemotactic response to urea, flurofamide (a potent urease inhibitor), sodium ion, and bicarbonate ion. These chemotactic responses are also observed in the viscous environment. Thus, it appears that H. pylori has chemotactic movement that is independent of urease activity. The chemotactic response was inhibited by carbonyl cyanide m-chlorophenylhydrazone (CCCP), a potent H+ pump inhibitor, but not by Na+ pump-inhibiting amiloride, suggesting this response is forced by H+-driven flagellar movement. Since urea and sodium bicarbonate are secreted from the gastric epithelial surface, this chemotactic response may contribute to the colonization by H. pylori and the persistence of its infection.