Antibody-dependent macrophage-mediated activity against Helicobacter pylori in the absence of complement.
Helicobacter pylori is a Gram-negative bacterium, which chronically infects the stomach. Little is known about the immune mechanisms limiting the spread of infection and/or contributing to protection after experimental immunization. In this study, we investigated the hypothesis that specific antibodies and host cells cooperate in the immunity against H. pylori. Antibody-dependent cellular activity against H. pylori was assessed using specific immune serum, or purified IgG, in an in vitro assay, with peritoneal cells as effector cells. The natural antibacterial activity of peritoneal cells was significantly augmented by H. pylori-specific antibodies in a dose-dependent manner. A novel finding was that this killing effect did not require functional complement. Most of the bactericidal activity was associated with cells that were adherent, DX5(-), CD19(-), CD11c(-), Thy-1.2(-), CD11b(+) and CD16/32(+), indicating that the main effector population was represented by macrophages. Similar antibacterial killing was obtained with the macrophage cell line GG2EE. Cytochalasin D significantly impaired this antibacterial activity, suggesting that phagocytosis plays a major role in the antibody-mediated H. pylori killing.
D000818:Animals; D000907:Antibodies, Bacterial / Q000276:immunology*; D000918:Antibody Specificity; D003165:Complement System Proteins / Q000502:physiology*; D005260:Female; D016480:Helicobacter pylori / Q000276:immunology*; D007074:Immunoglobulin G / Q000276:immunology; D008264:Macrophages / Q000276:immunology*; D051379:Mice; D008809:Mice, Inbred C3H
D000907:Antibodies, Bacterial; D007074:Immunoglobulin G; D003165:Complement System Proteins