Background: H. pylori is a causative agent of chronic gastritis. However, the pathogenic mechanism by which H. pylori induces chronic inflammation and epithelial injuries in the gastric and duodenal mucosa is not well known. Investigators have recently reported that some monoclonal antibodies against H. pylori cross-react with the gastric epithelial cells. So, there exists the possibility that the autoimmune mechanism may be involved in the pathogenesis of chronic gastritis caused by H. pylori. The purpose of his study is to investigate whether the antibodies against H. pylori react with human tissues or not, using a large panel of monoclonal antibodies.
Materials and methods: Two hundred and fourteen monoclonal antibodies against H. pylori were produced. An immunohistochemical staining of human tissues, including H. pylori-infected gastric mucosa, was performed using the antibodies.
Results: Of 214 monoclonal antibodies, 71 antibodies reacted with H. pylori in the gastric mucosa. Of 71 antibodies, 25 antibodies also reacted with gastric epithelial cells, 11 antibodies reacted with ductal cells of the salivary gland, 11 antibodies reacted with renal tubular cells, and 8 antibodies reacted with duodenal epithelial cells. The antibodies which showed cross-reactivity with gastric epithelial cells included those against urease, flagella, lipopolysaccharide, and heat shock protein of H. pylori.
Conclusions: It is believed that the autoimmune reaction might be involved in the pathogenesis of chronic gastritis due to H. pylori infection, and that the autoimmune reaction induced by H. pylori infection might also be involved in the pathogenesis of various diseases in other organs.