The researchers found that infection of the stomach by the bacterium Helicobacter pylori (H. pylori) leads first to mild inflammation. As the inflammation occurs, cells lining the stomach produce a specific kind of sugar molecule and display it on their surface. Normally, that sugar, known as sialyl-di-Lewis x (sLex), serves as a flag to attract immune cells to the infection site. The worse the inflammation, the more sLex the cells display.
The investigators also discovered, however, that H. pylori latches on to the new sugar using a previously unknown bacterial adhesin protein, enabling the bacteria to draw closer to the stomach cells, presumably where more nutrients are available. This worsens the inflammation and further increases the amount of sLex on the stomach cells. Some of the bacteria, which are loosely attached, may then move a microbial arms-length away from the cells and thereby avoid destruction by immune cells that are attracted to the increasing display of sLex. The investigators believe that the degree of inflammation may then subside enough that those bacteria that move in close again will have a good chance of survival and, once more, profit from the better nutrient supply.
"These findings should improve our understanding of how H. pylori infection happens, how our immune system responds to it, and how the bacteria cope with that response," says Douglas E. Berg, Ph.D., Alumni Professor in Molecular Microbiology and professor of genetics at the School of Medicine and co-author of the study. "We also hope that understanding how these adhesins w
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Contact: Darrell E. Ward
wardd@msnotes.wustl.edu
314-286-0122
Washington University School of Medicine
25-Jul-2002