MECHANISMS OF CELLULAR CYTOTOXICITY INDUCTION IN GASTRIC MUCOSAL INFLAMMATION

Abstract

Development and chronicity of inflammatory process in gastric mucosa may contribute to persistence of a number of microorganisms – Helicobacter (H.) pylori, Staphylococcus (S.) aureus, Candida species (spp.), Herpesvirus and others in the host organism. Many authors have recognized an important role of T helper (Th) type 1 and regulatory T cells in evolvement of gastritis, whereas importance of cytotoxic T lymphocytes (CTLs) is still to be confirmed. This review presents analysis of available scientific data about induction mechanisms of cellular cytotoxicity in inflammatory process affecting gastric mucosa. Bacterial populations, depending on their density, are able to regulate expression of genes encoding synthesis of protein virulence factors, thus accelerating adaptation for changing environmental conditions. Upon receptor-mediated recognition of characteristic microbial structures, i.e., pathogen-associated molecular patterns (PAMPs) and danger signals altered by stress, or cellular structures damaged by infectious pathogens (DAMPs), transcription factors are activated, thus leading to production of early pro-inflammatory interleukins (IL), interferons (IFN) type I and induction of immune responses. It is shown that the antigens of H. pylori and Candida spp. promote infiltration of mucosa gastric by activated CD8+CTLs, and Herpesvirus induce a significant increase in the number of perforin-positive (Pr+) CD8+ and CD16+ cells, phenotypic changes in CD4+lymphocytes, with acquisition of direct cytolytic activity.

Keywords

• t lymphocytes
• cell cytotoxicity
• interleukin
• interferon
• helicobacter pylori
• herpesvirus
• candida