H. pylori is a spiral-shaped bacterium that can live in the acidic environment of the stomach and duodenum which is the section of intestine below the stomach. It is the most common cause of ulcers of the stomach and duodenum, accounting for up to 90% of duodenal ulcers and up to 80% of gastric ulcers. Infection with H. pylori also causes gastritis, and infected persons also have a 2- to 6-fold increased risk of developing mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric cancer compared with uninfected counterparts.

H. pylori infection is common in the United States and is most often found in persons from lower income groups and older adults. About 20% of persons less than 40 years of age and about 50% of persons over 60 years of age are infected. Most infected people do not have symptoms and only a small percentage go on to develop disease.

Previous research has focused on the affects diet has on the stomach environment where H. pylori resides, but until now scientists have overlooked the response of the microorganism specifically to these dietary queues. Working from the epidemiological evidence that H. pylori infection combined with a high-salt diet results in an increased incidence of severe gastric maladies, Gancz and colleagues decided to look at the direct effect a high concentration of salt had on both the growth and gene expression of the bacterium.

"We noted that H. pylori growth rate shows a sharp decline at high salt concentrations. Moreover, bacterial cells exposed to increased salt exhibited striking morphological changes: cells became elongated and formed long chains," says Gancz. "We conclude that H. pylori exposed to high levels of salt in vitro exhibit a defect in cell division."

They also discovered transcription of two genes responsible for the virulence of the bacterium was increased during high-salt conditions. "The altered expression patterns of some virulence genes may partially explain the increased disease risk that is associated with a high salt diet in H. pylori infected individuals," says Gancz.

This work was supported by a grant from the U.S. National Institutes of Health.


SOURCE: American Society for Microbiology

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