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The journey on the road of discovery of Helicobacter pylori (Hp) to cure of infection associated conditions ended in Stockholm on December 10, 2005 when Barry Marshall and Robin Warren received the Nobel Prize in Physiology or Medicine. All who have traveled this road, both patients and physicians, should celebrate this journey with them. It was not an easy journey, at least not initially, since skeptics lined the path jeering travelers with chants that infectious ulcer disease and cancer lacked any scientific basis. Now at journeys end the skeptics are gone and the scientific world has embraced the clinical importance of H. pylori and is clamoring to capitalize on the opportunities presented by Marshall’s and Warren’s discovery. While prevalence of infection is declining, it’s clinical and scientific influence will remain prominent for decades. Hp infection causes varied clinical outcomes presumably due to variable intensity and distribution of gastritis and altered gastric acid physiology among infected individuals. Most pathogenic bacterial strains contain a specific cluster of genes know as the “cag pathogenicity island” which encodes for CagA protein and processes responsible for it’s translocation into host cells. Intercellular CagA induces pro-inflammatory cytokine production, interleukin-1b (IL-1 b) and interleukin-8 (IL-8), which activate and recruit acute inflammatory cells to the mucosa causing intense gastritis and modifying gastric acid secretion. Specific polymorphisms of the IL-1b gene cluster increase risk for stomach cancer. Presumably more severe gastric inflammation leads to repeated epithelial injury and repair, eventual mitotic errors, proliferation of chromosomally altered cells, and finally cancer. An alternative explanation for H. pylori associated gastric cancer proposes that the inflammatory milieu of the infected stomach promotes homing and engraftment of pluripotent bone marrow derived cells which in their foreign inhospitable environment exhibit altered growth and differentiation such that epithelial cancer develops.

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2006-11-08   |   1,277 visitas   |   Evalua este artículo 0 valoraciones

Vol. 71 Núm.1. Agosto 2006 Pags. 31-33 Rev Gastroenterol Mex 2006; 71(Supl. 1)