But now Amieva and his colleagues have identified a protein that regulates H. pylori’s ability to seek shelter. The protein could be a target for therapies that specifically combat H. pylori while leaving our friendly gut bacteria alone. The findings were published on July 26 in the journal mBio.
H. pylori makes a living in about half the people on Earth. For most, the tiny tenants go unnoticed. But in about 15 percent of those infected, the microbes cause ulcers. Yet worse, for others, it increases the risk of gastric cancer.
Despite the fact that it lives in our stomachs, H. pylori is a not fan of our caustic digestive acids. To avoid getting burned, the bacteria use their propeller-like appendages called flagella to power their corkscrew bodies through the mucous that protects our stomach cells. While it was known that the bacteria colonize the stomach’s surface mucus, the researchers found that they also take up residence deep in some of the glands that tunnel down from the stomach’s surface.
The team made the discovery while studying a protein called ChePep. Michael Howitt, PhD, a former graduate student in Amieva’s lab, created a special strain of H. pylori that cannot make the protein. Bacteria lacking ChePep don’t make their way down into the glands, prompting Howitt to examine how the bugs move.
