The influence of Helicobacter pylori presence on the immunophenotype of inflammatory infiltrate in gastric diseases.

The first medical hypothesis about the possible relationship between chronic inflammatory response and carcinogenesis belongs to Virchow and it was published in 1893. In these days, multiple studies demonstrate the certain involvement of chronic inflammation as trigger of progression towards malignancy. The fact that in 1994, the International Agency for Research on Cancer considered Helicobacter pylori as first class carcinogenic agent, is postulating the existence of the pathogenical chain carcinogenesis, of chronic inflammatory lesions as it was described by Correa, as a first step. Our study including 75 patients who underwent surgical procedures for gastric lesions uses immunohistochemical studies for lymphocytes phenotyping, to identify the nature of inflammatory cells involved, correlating the results with the presence of Helicobacter pylori. We tried to bring new information needed for establish to what extent the chronic inflammation of gastric mucosa is a response to the presence of bacteria and is implicated in tumorigenesis. We used T cells antibodies: CD3, CD4, CD5, CD8, CD57, GranzymeB and B cells antibodies: Cd20 and CD23. Our results revealed the presence of immune cellular response to Helicobacter pylori in gastric mucosa, based on T helper, cytotoxic and NK cells. B cells have a minor role in this response. CD4+ cells seem to be involved in local protection response as well as in carcinogenesis, while CD8+ have a minor or no role in carcinogenesis.