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CONTACT:      Jim Sliwa

jsliwa@asmusa.org

(202) 942-9297

May 21 – 25, 2007: (416) 585-3716

 

 

EMBARGOED UNTIL: Tuesday, May 22, 2007, 9:00 a.m. EDT

 

 

 

TORONTO – May 22, 2007 -- Scientists have identified yet another risk from a high-salt diet.  High concentrations of salt in the stomach appear to induce gene activity in the ulcer-causing bacterium Helicobacter pylori, making it more virulent and increasing the likelihood of an infected person developing a severe gastric disease.

 

“Apparently the stomach pathogen H. pylori closely monitors the diets of those people whom it infects.  Epidemiological evidence has long implied that there is a connection between H. pylori and the composition of the human diet.  This is especially true for diets rich in salt,” says Hanan Gancz, of the Uniformed Services University of the Health Sciences in Bethesda, Maryland, who presents the research May 22, 2007 at the 107th General Meeting of the American Society for Microbiology in Toronto.

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 transciption 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.

 

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More information on this and other presentations can be found online in the 107th ASM General Meeting Press Kit at index.php?option=com_content&view=article&id=50000 or by contacting Jim Sliwa (jsliwa@asmusa.org) in the ASM Office of Communications. The phone number for the General Meeting Press Room is (416) 585-3716 and will be active from 12:00 noon EDT, May 21 until 12:00 noon EDT, May 25.

 

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