N-acetylcysteine prevents the development of gastritis induced by Helicobacter pylori infection
The discovery of Helicobacter pylori as an important gastric pathogen and as one of the most common bacterial infections, now more than a decade ago, completely changed our concepts of both gastroduodenal disease and the immunobiology of the stomach. At this moment, H. pylori is recognized as the cause of chronic gastritis, peptic ulcer disease, and as an important causal factor in the chain of events leading to gastric carcinoma. Before H. pylori can lead to gastritis and a chronic immune response the bacterium has to evade and subsequently to interact with the mucosal defence mechanisms. After colonization of the gastric mucosa by H. pylori the persistent presence and survival of the bacterium leads to a chronic local and systemic immune response. Recent developments and insights into the gastric mucosal inflammation caused by H. pylori and its pathogenic mechanisms are the subject of this review.