Modulation of phagocyte apoptosis by bacterial pathogens.
Phagocytic leukocytes such as neutrophils and macrophages are essential for the innate immune response against invading bacteria. Binding and ingestion of bacteria by these host cells triggers potent anti-microbial activity, including production of reactive oxygen species. Although phagocytes are highly adept at destroying bacteria, modulation of leukocyte apoptosis or cell death by bacteria has emerged as a mechanism of pathogenesis. Whereas induction of macrophage apoptosis by pathogens may adversely affect the host immune response to infection, acceleration of neutrophil apoptosis following phagocytic interaction with bacteria appears essential for the resolution of infection. This idea is supported by the finding that some bacterial pathogens alter normal phagocytosis-induced neutrophil apoptosis to survive and cause disease. This review summarizes what is currently known about modulation of phagocyte apoptosis by bacteria and describes a paradigm whereby bacteria-induced neutrophil apoptosis plays a role in the resolution of infection.
DeLeo
F R
FR
Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA. fdeleo@niaid.nih.gov
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001419:Bacteria / Q000254:growth & development*; D006801:Humans; D007239:Infections / Q000503:physiopathology; D008264:Macrophages / Q000382:microbiology / Q000502:physiology; D008954:Models, Biological; D009504:Neutrophils / Q000382:microbiology / Q000502:physiology; D010586:Phagocytes / Q000382:microbiology / Q000502:physiology*; D017382:Reactive Oxygen Species / Q000378:metabolism
D017382:Reactive Oxygen Species