title: Antibacterial defence mechanisms.
abstract: Pathogenic bacteria fall into two groups with regard to their fate within phagocytes: extracellular bacteria are promptly killed after phagocytosis and facultative intracellular bacteria are resistant to intracellular killing unless macrophages are activated. Extracellular bacteria cause purulent infections, and facultative intracellular bacteria granulomatous ones. Humoral immune mechanisms (antibody, complement) deal mainly with extracellular bacteria, while cellular immune mechanisms (T cells, macrophages) deal with facultative intracellular bacteria. The specific and nonspecific factors and their interactions are discussed with respect to their role in the buildup of an effective antibacterial defence.
mesh_terms: D000917:Antibody Formation; D001424:Bacterial Infections / Q000276:immunology*; D002450:Cell Communication; D003176:Complement C3 / Q000276:immunology; D006099:Granuloma / Q000209:etiology; D006648:Histocompatibility; D006801:Humans; D007116:Immunization, Passive; D007074:Immunoglobulin G / Q000276:immunology; D007375:Interleukin-1 / Q000276:immunology; D007376:Interleukin-2 / Q000276:immunology; D008088:Listeriosis / Q000473:pathology; D008222:Lymphokines / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D009504:Neutrophils / Q000276:immunology; D009895:Opsonin Proteins / Q000276:immunology; D010587:Phagocytosis; D013601:T-Lymphocytes / Q000276:immunology / Q000637:transplantation
chemical_list: D003176:Complement C3; D007074:Immunoglobulin G; D007375:Interleukin-1; D007376:Interleukin-2; D008222:Lymphokines; D009895:Opsonin Proteins