Suppression of human mononuclear cell response byHelicobacter pylori: Effects on isolated monocytes and lymphocytes

Abstract

Helicobacter pylori colonization of the human gastric mucosa causes a long-term, not self-limiting inflammation, suggesting that the microbe has properties to protect itself against the host immune defence system. Recently we were able to demonstrate that H. pylori suppresses the in vitro proliferative response of human peripheral blood mononuclear cells to antigens as well as to mitogens without affecting cell viability. The purpose of this study was to clarify which cell subsets of mononuclear cells are influenced by H. pylori. The use of monocytes which had been pretreated with a soluble cytoplasmic fraction of H. pylori (30 micrograms ml-1) led to a suppressed proliferation of T cells after PHA-activation. Activation of isolated T cells with PHA and PMA revealed that the proliferative response of lymphocytes could also be inhibited independently of monocytes. The anti-proliferative effect was associated with a reduction of IL-2 receptor (CD25) expression as well as an inhibition of blastogenesis. Furthermore, the spontaneous proliferation of EBV-transformed B cell lines was suppressed in a dose-dependent manner. FACS-analysis of HLA-DR, ICAM-1 and CD14 expression on the surface of monocytes revealed an influence of H. pylori on CD14 expression at a concentration of 30 micrograms ml-1, while the expression of HLA-DR and ICAM-1 was not affected at this concentration.

Historical and Molecular Perspectives on the Presence of Helicobacter pylori in Latin America: A Niche to Improve Gastric Cancer Risk Assessment

“…Several studies have demonstrated that H. pylori affects immune infiltration, mainly by impairing proliferation or promoting apoptosis in T-cells [65][66][67]. In addition, gastric epithelial cells constitutively express class II Major Histocompatibility Complex molecules and may display a role as secondary antigen-presenting cells; however, the VacA toxin can impair the presentation of the Major Histocompatibility Complex-antigen [68].…”