Helicobacter pylori: A member of the normal gastric microflora or a dangerous carcinogenic microorganism?

Helicobacter pylori is a Gram-negative, microaerophilic bacterium, that colonizes the human gastric mucosa at a rate which is globally, between 10-35% in developed countries and 70-90% in underdeveloped countries. It has coevolved with man in the last 250,000 years, and followed its human host in its subsequent exit from Africa nearly 60,000 years ago. Its presence in our primitive ancestors illustrates a paradigm of successful symbiosis, possibly conferring protection to the gastric mucosa from the strongly acidic pH, by increased secretion of bacterial urease. In our contemporary times, infection with H. pylori usually occurs early in childhood, especially within the first 5 years and although the majority of patients are asymptomatic, H. pylori infection remains the main causative agent for the development of chronic active gastritis and peptic ulcer disease throughout adulthood. More specifically, on the background of chronic active gastritis, a 10-15% of adult patients develop gastric or duodenal ulcers. Moreover, 0.5%-2.0% of adult carriers by the age of 60yo, develop gastric adenocarcinoma and MALT-lymphoma (Mucosa-Associated Lymphoid Tissue lymphoma). Based on such epidemiologic observations in 1994 the World Health Organization classified H. pylori as "first-class carcinogenic agent". In general, H. pylori pathogenesis appears to be determined by the interaction of specific cytotoxic bacterial factors, combined with host genetic polymorphisms which dictate the extent and duration of immune response towards the infection, as well as environmental factors such as diet and smoking etc. For this reason, the study of H. pylori infection is extremely useful for understanding both the general mechanisms of pathogenesis of chronic infectious diseases as well as, the relationship between pro-inflammatory mechanisms and carcinogenesis in the epithelium. Research in our laboratory focuses on the effect of bacterial virulence factors in the clinical pathology of symptomatic patients with H. pylori infection. More specifically, we work towards the elucidation of molecular mechanisms by which virulence factors may modify intracellular signaling pathways in gastric epithelial cells and their contribution in the inflammatory process in the lamina propria of gastric tissue.

Speaker: Dionyssios Sgouras
Principal Investigator, Hellenic Pasteur Institute
Time: Wednesday, 16 May 2012, 13:00