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New mechanism of Helicobacter infections decoded
Infection with the Helicobacter pylori bacterium is one of the most common causes of stomach ulcers and stomach cancer. So far, however, it has not been clear what mechanism the bacterium is involved in causing the disease. Scientists have now succeeded in identifying a pair of molecules in two independent studies that have a significant influence on the pathological effect of the bacterium. The researchers hope that their results will enable better treatment and prevention in the future.
In their current studies, the scientists at the Ludwig Maximillians University (LMU) in Munich, the Technical University of Munich (TUM) and the University Hospital Essen were able to decrypt "the crucial molecules and processes" of Helicobacter infection and thus identify new treatment options Communication from the German Center for Infection Research (DZIF). DZIF researchers were instrumental in both studies. The work was published in the specialist journal "Nature Microbiology".
Helicobacter pylori often cause stomach ulcers and stomach cancer
Infections with Helicobacter pylori are in many cases triggers for the development of stomach ulcers and stomach cancer. "Chronic Helicobacter infection of the epithelial cells of the gastric mucosa is considered an important risk factor for stomach cancer," reports the DZIF. Around 750,000 new stomach cancers are reported worldwide each year. So far, it has not been clear which mechanism in Helicobacter infection promotes the development of stomach ulcers and stomach cancer.
Previously unknown pair of molecules discovered
To better understand the mechanisms of Helicobacter infection, the researchers led by Prof. Rainer Haas from the Max von Pettenkofer Institute at LMU, Professor Markus Gerhard from the Institute for Medical Microbiology, Immunology and Hygiene at TUM and Dr. Bernhard B. Singer from the University of Duisburg-Essen, which receptors are involved in the binding between bacterium and host cell. The researchers were able to identify previously unknown receptors on the surface of the epithelial cells (so-called CEACAMs) to which the bacteria dock. They were also able to determine the counterpart on the bacterial side - the HopQ protein.
Bacteria with a molecular lethal injection
The researchers also found that the pair of molecules discovered “is (not only important for the binding of the bacteria to their host cells), but also for the pathogenic effects of the bacteria,” said the DZIF. The actual disease trigger is the bacterial protein CagA, which is injected by particularly pathogenic H. pylori strains via a needle-like extension into the epithelial cells of the gastric mucosa. The “molecular lethal injection” forms the basis for the feared effects of the bacteria. The molecular injection system only becomes active when the bacterial protein binds to the proteins of the epithelial cells.
New options for prevention and therapy?
Based on the discovered mechanism, the researchers believe that new therapy options could open up in the future. Prof. Gerhard assumes that the bacterial molecule HopQ can be used diagnostically and therapeutically. A soluble variant of HopQ or parts of the protein could possibly prevent the bacterium from binding to the gastric cells and thus counteract the process of developing the disease. "Specific inhibitors of the HopQ-CEACAM interaction could either completely prevent infection or prevent the CagA injection," emphasizes Prof. Haas in a press release from the LMU on the research results.