May 15, 2008 The bacterium Helicobacter pylori infects various parts of the stomach and small intestine, and chronic infection with H. pylori can cause stomach cancer. New insight into the mechanisms by which H. pylori modulates human stomach cells to increase its chances of successfully infecting those cells has been provided by Celso Reis and colleagues, at the University of Porto, Portugal.
To successfully infect the stomach H. pylori must adhere to the cells lining the stomach. One way in which it does this is to induce the cells lining the stomach to express a molecule known as sialyl--Lewis x, which binds to the H. pylori protein SabA. In the study, H. pylori was found to modify the expression of many genes by a human stomach cell line. However, the extent of the modification depended on how good the strain of H. pylori was at causing disease, those good at causing disease modified gene expression to a greater extent.
Further, only those good at causing disease modified the expression of the gene carrying the information needed to make the protein beta-3GnT5, which is required for making sialyl--Lewis x. As cells engineered to express beta-3GnT5 showed increased expression of sialyl--Lewis x and increased adhesion to H. pylori, the authors concluded that they had uncovered one mechanism by which H. pylori modulates human stomach cells to increase its chances of establishing an infection.
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- Helicobacter pylori induces beta-3GnT5 in human gastric cell lines, modulating expression of the SabA ligand sialyl--Lewis x. Journal of Clinical Investigation. May 15, 2008.
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