The Effect of Helicobacter pylori Eradication Treatment on the MUC 1 and Lewis Antigens Level in Human Gastric Juice: Preliminary Study

Abstract

Helicobacter pylori is considered as a causative agent of gastritis, duodenal and gastric ulcers, and gastric cancer. During inflammation, association of the pathogen of gastric epithelial cells and mucins is considered important. It was postulated that Lewis b structures of secretory MUC 5AC mucin can be a receptor for the bacterium. Some authors also suggest that epithelial MUC 1 mucin may be implicated in the mechanism of infection. The main aim of our work was to support this last suggestion by evaluation of the possible changes in MUC 1 and Lewis a and b levels in gastric juice before and at the end of eradication treatment. The gastric juices of ten examined patients were chromatographed on a Sepharose 4 B column, electrotransferred on Immobilon P membranes, and assessed for MUC 1 and Lewis a and b structures using monoclonal antibodies. In 90% of examined patients, higher amounts of MUC 1 mucin were observed at the end of eradication treatment. Similar results for Lewis a and b structures were found. In the case of MUC 1 and Lewis b, the differences were statistically significant. Helicobacter pylori influences expression of the soluble form of MUC 1 mucin and Lewis a and b structures present in gastric juice.