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Our mucosal surfaces are constantly exposed to numerous bacterial species, some of which can induce DNA damage in host cells. Normally this remains inconsequential, as the rapid turnover of the mucosa means damaged cells are shed within days. However, if the long-lived stem cells that continually give rise to new replacement cells receive damage it could lead to the development of cancer. Researchers at the Max Planck Institute for Infection Biology and the Charité-Universitätsmedizin in Berlin have now revealed that the gastric stem cell pool does do not merely divide to generate new daughter cells, but that they can secrete antimicrobial molecules to actively defend the stem cell niche against bacteria.
The team looked at infections with the gastric pathogen Helicobacter pylori, a bacterium which chronically colonizes the stomach of around half the world's population, and is known to cause stomach cancer. Michael Sigal of the Charité, who led the study with the Max Planck team of Thomas F. Meyer, previously showed that the bacterium not only colonizes the surface of the gastric epithelium but is able to penetrate deep into the base of gastric glands, where the stem cells reside.
Response - Infection - Cells - Tissue - Amounts
In response to the infection, the stromal cells of the underlying connective tissue produce increased amounts of a factor called R-spondin, which enhances the activity of the so-called Wnt pathway—an almost universal driver of stem cell turnover in various tissues. In response, the stem cells increase their turnover, leading to hyperplasia, a thickening of the mucosal lining that is typical for patients with gastritis.
Although the team saw that R-spondin led to a drop in the number of colonizing bacteria, they were not convinced that...
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