The Progress in Helicobacter Pylori High Risk Pathogenic Marke

Abstract

It has been widely accepted that Helicobacter pylori was closed related with tumorigenesis of gastric cancer, but the pathogenic factor of this bacteria as well as the intrinsic mechanism are still unclear. We analyzed the proteomics of Helicobacter pylori strains isolated from both gastritis and gastric cancer and discovered several differential proteins. Among these proteins the Thioredoxin-1 (Trx-1) was considered most significant. Trx-1 protein has an anti-oxidative function and might increase cellular proliferation and anti-apoptosis. It helped to protect Helicobacter pylori from the oxidative reaction from the host so as lead to the long term colonization. We carried out a series of researches on this protein. The results revealed that Trx-1 was highly expressed in Helicobacter pylori isolated from cancer patients compared with the bacteria from gastritis patients. In cell culture study, up-regulation of Trx-1 expression in GES-1 and BCG823 cell lines might increase cell growth and promote cells into S phase. What's more, infected with Helicobacter pylori that express high level Trx-1 might induced cell apoptosis, decreased the expression of cyclin D1 and upregulated p21 in GES-1 cell line, while increase cell proliferation, and upregulate cyclin D1 in BCG823 cell line, indicating an oncogenic effects. We further infected Mongolian gerbils by Helicobacter pylori with high level Trx-1. The results showed long term infection lead to serious pathologic change of the stomach mucosa and finally adenocarcinoma occurred. In conclusion, Helicobacter pylori Trx-1 may play an important role in the development of stomach adenocarcinoma and can be considered as pathogenic marker. Future studies are still necessary for the specific process of Trx-1 protein on gastric mucosal after H. pylori infection, the relationship between clinical TNM stages and Hp Trx-1 level, as well as the downstream signal pathways that are involved in the carcinogenic process.