Immune suppressive effects of Helicobacter pylori on human peripheral blood mononuclear cells.
Helicobacter pylori, the causative agent of type-B gastritis and duodenal ulcer in man is described as a bacterium able to stimulate the human immune system. This study demonstrates that H. pylori besides this property possesses an immune suppressive activity. The in vitro proliferation of human peripheral blood mononuclear cells to purified protein derivative of tuberculin (PPD), phytohemagglutinin, and concanavalin A was reduced in a dose-dependent manner by bacteria which had been inactivated by incubation at 56 degrees C as well as by a soluble cytoplasmic fraction of H. pylori. The immune suppressive effect on the mitogen-induced proliferation could be increased by preincubation of the mononuclear cells with H. pylori. The observed effect does not seem to be a specific phenomenon depending on prior exposure of the blood donors to H. pylori, since suppression occurred with mononuclear cells of H. pylori-infected patients as well as of antibody-negative healthy control individuals. The suppressive activity was non-dialyzable, heat-labile (100 degrees C, 30 min) and sensitive to trypsin. Furthermore, the treatment at 100 degrees C caused an increase in the capability of H. pylori to induce lymphoproliferation. This fact indicates that the suppressive factor is also effective on H. pylori antigens. While exogenous interleukin-2, could to a certain extent, restore the responsiveness of the lymphocytes after PPD-stimulation in the presence of H. pylori, the addition of interleukin-1 had no effect on the suppressed lymphoproliferation. Cell-separation and cell-mixing experiments indicated that an influence on monocytes rather than on T cells is the major cause of the observed suppressive effect. Although the immunological mechanisms involved in H. pylori-associated gastritis are not clearly defined, it is reasonable to presume that suppression of host defense mechanisms may contribute to the pathogenesis of this disease.
Knipp
U
U
Department of Medical Microbiology and Immunology, Ruhr-Universität Bochum, Germany.
Birkholz
S
S
Kaup
W
W
Opferkuch
W
W
D002469:Cell Separation; D002478:Cells, Cultured; D003208:Concanavalin A / Q000276:immunology; D016481:Helicobacter Infections / Q000276:immunology*; D016480:Helicobacter pylori / Q000276:immunology*; D006801:Humans; D007111:Immunity, Cellular; D015850:Interleukin-6 / Q000096:biosynthesis; D008213:Lymphocyte Activation / Q000276:immunology; D009000:Monocytes / Q000276:immunology*; D010835:Phytohemagglutinins / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*; D014373:Tuberculin / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D015850:Interleukin-6; D010835:Phytohemagglutinins; D014373:Tuberculin; D014409:Tumor Necrosis Factor-alpha; D003208:Concanavalin A