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Microarrays identify strain-specific features of Helicobacter pylori that influence stomach inflammation
By Bijal P. Trivedi

Researchers are using whole-genome microarrays to understand how genetic differences between strains of the stomach bacterium Helicobacter pylori influence the severity and type of disease. H. pylori is one of the most common bacteria, infecting two-thirds of the world's population. The bacterium causes up to 80 percent of stomach ulcers and about 90 percent of duodenal ulcers worldwide. Infections can result in a range of conditions, from heartburn and nausea to stomach inflammation to ulcers to stomach cancer.

Richard Peek, of Vanderbilt University School of Medicine, in Nashville, Tennessee, and colleagues compared infections caused by two strains of H. Pylori—G1.1 and B128. The B128 strain is more likely to lead to gastric cancer. When the researchers infected Mongolian gerbils with the bacteria they found that B128, a gastric ulcer strain, causes more severe inflammation than the duodenal ulcer strain G1.1.

A comparison of the genes carried by the two strains revealed significant differences. The B128 strain carries 26 out of the 27 genes that make up the cag pathogenicity island: a group of genes known induce an inflammatory response. G1.1, by contrast, only carries 7 of these 27 genes.

Peek's team modified the B128 strain by removing two genes from the pathogenicity island and found that gerbils infected with this altered strain showed far less inflammation. The microarray strategy enabled the researchers to identify genetic components that influence specific aspects of the host disease response.

H. pylori is a spiral shaped bacterium that lives in the mucous lining of the stomach, which protects it from the harsh acidic environment. The complete genome sequences for two strains of H. pylori were published in the late 1990s.

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Israel, D.A. et al. Helicobacter pylori strain-specific differences in genetic content, identified by microarray, influence host inflammatory responses. J Clin Invest 107, 611-620 (March 2001).

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