Scientists have determined that decay-accelerating factor (DAF), a protein found in epithelial cells in the stomach, acts as a receptor for the bacteria Helicobacter pylori. Blocking this interaction could lead to new drugs that reduce the risk of peptic ulcer disease or gastric cancer.
The research appears as the "Paper of the Week" in the May 12 issue of the Journal of Biological Chemistry, an American Society for Biochemistry and Molecular Biology journal.
Helicobacter pylori are spiral shaped bacteria that live in the thick layer of mucus that covers the stomach lining. The bacteria are found everywhere in the world, but are especially prevalent in developing countries, where up to 80% of children and 90% of adults can have laboratory evidence of an H. pylori infection--usually without having any symptoms.
The vast majority of H. pylori in colonized hosts are free-living, but approximately 20% bind to gastric epithelial cells. This binding induces an immune response and alters the morphology and behavior of the epithelial cells due to injection of bacterial proteins into the cells. This interaction can lead to peptic ulcer disease, gastric adenocarcinoma, and non-Hodgkins lymphoma of the stomach.
"Ulcers are a breach in the gastric or duodenal mucosa and gastric adenocarcinoma is one type of cancer of the stomach," explains senior author Dr. Richard M. Peek, Jr. of the Vanderbilt University School of Medicine. "H. pylori alters acid production and can lead to increased acid outputs which causes peptic ulcer disease. The means through which H. pylori causes gastric cancer are more complex but likely involve alterations in gastric epithelial cell responses that are perturbed within the context of a chronic gastric inflammatory infiltrate, which can persist for decades."