It has been almost 20 years since the first report that infection with the bacterium Helicobacter pylori increases the risk of stomach ulcers. Now a team of Japanese scientists report in the March issue of Nature Genetics that a receptor on stomach cells for a toxin produced by H. pylori mediates the signals that lead to ulceration in mice. The findings could have implications for developing treatments. The H. pylori protein VacA has been singled out as a culprit for causing disease. VacA binds to several receptors on stomach cells to gain entry into the cells and cause damage. Masaharu Noda and colleagues at the National Institute for Basic Biology in Okazaki, Japan engineered mice deficient in one of the VacA receptors--the protein tyrosine phosphatase receptor type Z (Ptprz). While 10 out of 12 mice developed ulcers after being fed VacA, none of the mice lacking Ptprz did. VacA was still able to get inside stomach cells (probably via other receptors), but without Ptprz it could not transmit its toxic signals for causing ulcers.
About 50% of the world's population is infected with H. pylori. Identifying the proteins that mediate H. pylori infection and disease could contribute to the development of vaccines against stomach ulcers, according to Richard M. Peek of Vanderbilt University School of Medicine in an accompanying News and Views article.
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