In human gastric tissue, however,
gastric epithelial cell proliferation is significantly higher but apoptotic indices are lower among persons colonized with cag + compared to cag - strains or uninfected persons leading us to postulate that reduced rates of cell loss, when accompanied by hyperproliferation, may heighten retention of mutagenized cells, which could predispose towards cancer.
Once the bacterial cell signaling protein cagA reaches the host cytosol, it is capable of altering subsequent generations of progenitor cells, leading to the development of cancer through changes in mitotic activity, apoptosis, cellular assembly, and signaling.26 Although it should be noted that while the presence of the cagA protein doubles the risk of gastric cancer, cagA - negative strands also increase the risk of distal gastric cancer.27 Additional H pylori virulence factors include babA2, which encodes bacterial adhesion with
gastric epithelial cells, and vacuolating cytotoxin A, which is encoded by the gene vacA.28, 29 H pylori strains carrying some combination of the babA2, cagA, and vacA genes were associated with the highest risk of developing intestinal metaplasia.
The virulence effects of H pylori have been shown to derive from bacterium factors causing alterations in
gastric epithelial cells.
Adherence of H. pylori to
gastric epithelial cells is critical for induction of inflammation and injury; therefore, the overarching theme for our research has been delineation of the molecular signaling events initiated by bacterial: epithelial cell contact that regulate phenotypes related to carcinogenesis.
Acid secretion by
gastric epithelial cells is related to the physiologic function of oxyntic cells, which are called parietal cells.
These studies clearly provided evidence that GABA had a considerable gastroprotective effect on ethanol - induced gastric mucosal injury and
gastric epithelial cells injury.
Not exact matches
Increasing Metabolism and Digestive Efficiency Other research suggests that capsaicin causes the stomach's
epithelial cells to secrete more
gastric mucus, the glycoprotein which lubricates food masses and facilitates their movement throughout the stomach.
But the pH - responsiveness also allows the bacterium to escape a certain death by detaching from
epithelial - and mucus
cells that are shed into the
gastric juice,» says Jeanna Bugaytsova, researcher at Department of Medical Biochemistry and Biophysics and first - author of the article.
In order to ensure permanent survival in the human stomach, Helicobacter pylori must attach to the
epithelial cells in the
gastric mucosa.
High - salt diet induces
gastric epithelial hyperplasia and parietal
cell loss, and enhances Helicobacter pylori colonization in C57BL / 6 mice.
In laboratory studies apple polyphenol extracts were found to prevent damage to human
gastric epithelial (intestinal wall)
cells.