Findings give hope for H. pylori vaccine.(Brief Article)

2002 SEP 11 - (NewsRx.com & NewsRx.net) -- The bacterium that causes stomach inflammation (gastritis), peptic ulcers and gastric cancer thrives in the human stomach by triggering changes in stomach cells and using those changes to its own advantage, say researchers in Sweden and at Washington University School of Medicine in St. Louis, Missouri. Their study appears in the journal Science.

The researchers found that infection of the stomach by the bacterium Helicobacter 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," said Douglas E. Berg, PhD, alumni professor in molecular microbiology and professor of genetics at the School of Medicine and coauthor of the study. "We also hope that understanding how these adhesins work will lead to a vaccine against H. pylori infections and to new drugs to treat or diminish their severity."

The findings also could help explain why the stomach inflammation that often accompanies the infection periodically flares up, then subsides, and why the infection persists for so long, said Berg, who also is a member of the tumor immunology program at the Alvin J. Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine.

"The ability of H. pylori to adjust its adherence properties to the level of inflammation it causes at the stomach surface could help explain how this bacterium maintains its persistent, decades-long infection in the stomach of millions worldwide," said lead investigator Thomas Boren, DDS, PhD, assistant professor of odontology and oral microbiology, at Umea University, Umea, Sweden.