Mechanisms of paralysis and apoptosis of the inflammatory cells in Helicobacter pylori infection

摘要: It is well established that Helicobacter pylori implicated as a causal agent of active chronic gastritis and peptic ulcer disease in humans1–4. However, although H. clearly pathogenic, most those infected are clinically silent or asymptomatic subjects. To this end, the basis for differing clinical manifestations affected with pylori, including gastric duodenal ulceration, atrophic superficial gastritis, unclear. Hence, it has been hypothesized individuals vary their immune recognition effector mechanisms directed towards organism. Thus, vigorous inflammatory response mediated by activated neutrophils, macrophages CD4+CD25+ T cells may result substantial mucosal injury5,6. In contrast, down-regulation inflammation CD8+ cells7, antigen-induced anergy8 apoptosis9 diminish acute to organism less damage. test hypothesis whether apoptosis plays role limitation infection first necessary establish residing epithelium lamina propria subjected regulation molecules governing apoptosis. A central pathway leading cellular lymphocytes initiated Fas, ~50kDa widely distributed surface receptor belonging TNF family10.