Urease Plays an Important Role in the Chemotactic Motility of Helicobacter pylori in a Viscous Environment

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.

Survival of Helicobacter pylori in gastric acidic territory

“…Some chemicals that are continuously secreted from the gastric epithelial cells to the lumen such as urea, 72 sodium carbonate, 73 and potassium carbonate 74 serve as potent attractants for H. pylori toward higher pH. Despite these data, little is known about the chemotactic behavior of H. pylori at various pH levels of the stomach, ranging from highly acidic to pH 4.5-6.5, which is the ecological niche of this bacterium.…”

Identification of the urease operon in Helicobacter pylori and its control by mRNA decay in response to pH

“…At the onset as well as during the course of infection, H. pylori may encounter gastric acid that kills most of the bacteria. The microorganism produces urease to a concentration of up to 6% of soluble proteins (Hu and Mobley, 1990) and has the ability to move towards urea in a viscous environment (Nakamura et al, 1998). Urease (urea amidohydrolase; EC 3.5.1.5) catalyses the hydrolysis of urea to yield ammonia and carbamate, and the latter compound is spontaneously decomposed to yield another molecule of ammonia and carbonic acid.…”

Random mutagenesis to identify novelHelicobacter mustelaevirulence factors

“…Urease is an important virulence factor in H. pylori and is essential for gastric colonization (Tsuda et al, 1994;Andrutis et al, 1995). It has been suggested that H. pylori senses gradients in urea which allow the bacteria to move towards the epithelial cells by chemotaxis; this offers an explanation for the decrease in adherence observed in our model for this mutant (Nakamura et al, 1998;Yoshiyama & Nakazawa, 2000). This may also explain the phenotype of mutant HM10, which was affected in an ORF homologous to the aspS gene, which is downstream of the cheV chemotaxis gene.…”