New findings raise the prospect of vaccine against ulcers
Thursday, July 25th 2002, 12:00 am
By: News On 6
WASHINGTON (AP) _ Researchers have discovered that the bacteria that cause ulcers attack the stomach by grabbing onto cells that are supposed to help the body's immune system.
Knowing this may help scientists design a vaccine to block the bugs, researchers believe.
An estimated half of the world's population is infected with Helicobacter pylori, a tenacious bacteria that can cause gastritis, stomach ulcers and has been associated with stomach cancer.
A research team led by Thomas Boren of Umea University in Umea, Sweden, found that H. pylori has developed a unique method to adhere to the stomach wall. The findings are published in Friday's issue of the journal Science.
When the surface of the stomach is first infected it becomes inflamed and displays a special kind of sugar molecule, called sLex, which normally serves as a flag to attract immune cells.
``The purpose is to signal ... that there is a part of the body that is in need of help, and that it would now be a good idea to send some more white blood cells over for assistance,'' explained Boren.
``Unfortunately,'' he added, ``H. pylori is most adaptive and has instead developed tools to utilize the new sugars displayed to its benefit ... for even better adhesion to the stomach cells.''
This results in heavier inflammation and peptic ulcer disease, Boren said.
But because the special adhesion proteins developed by H. pylori _ called BabA and SabA _ are only made by that bacteria, they may also prove to be its undoing.
This unique trait makes them ``prime candidates for a vaccine that would be specific for Helicobacter and would not affect any other bacteria,'' Boren said.
That's important because the gastrointestinal tract contains lots of bacteria, many of them beneficial.
Co-author Douglas E. Berg of the Washington University School of Medicine in St. Louis said the findings improve the understanding of the body's response to infection and how the bacteria copes with it.
``We also hope that understanding how these adhesins work will lead to a vaccine against H. pylori infections and new drugs to treat or diminish their activity,'' he said.
Currently antibiotics are often used to treat H. pylori infections, but Boren worries that if their use is too widespread, the bacteria will become resistant.
Boren said the goal is to develop a form of the two adhesion proteins that will provoke an immune response, preparing the body to recognize them and use them to target the bacteria for attack. Experiments are under way using mice, he said.
``Vaccine against Helicobacter and peptic ulcer disease has turned out to be a challenging task,'' he said, and even if things go well it would be six to eight years before the vaccine would be available to people.
The research may also help explain why infection with H. pylori sometimes seems to become milder and then worsens.
They found that the adhesin allows the bacteria to draw close to the stomach wall, where it worsens the inflammation. When this attracts more immune cells, the bacteria can draw away slightly, avoiding the immune attack and allowing the inflammation to subside _ and then draw in close again.
Dr. Stuart A. Thompson of the Medical College of Georgia, who was not part of the research team, noted that ``one of the main questions about Helicobacter is how it's able to exist in a state of chronic inflammation in the stomach.''
They have proposed an interesting mechanism ``where the germs adhere to the stomach wall, possibly to get nourishment, but can release partway to avoid immune cells,'' he said.