Phagocytosis induces superoxide formation and apoptosis in macrophages.
- Author:
Jae Bong PARK
1
Author Information
1. Department of Biochemistry, College of Medicine, Hallym University, Ockchon 1, Kangwon-do 200-702, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't ; Review
- MeSH:
Animals;
Apoptosis/*physiology;
Human;
Macrophages/*cytology/*metabolism;
NADPH Oxidase/metabolism;
Phagocytosis/*physiology;
Reactive Oxygen Species/metabolism;
Superoxides/*metabolism;
Support, Non-U.S. Gov't
- From:Experimental & Molecular Medicine
2003;35(5):325-335
- CountryRepublic of Korea
- Language:English
-
Abstract:
Phagocytosis by inflammatory cells is an essential step and a part of innate immunity for protection against foreign pathogens, microorganism or dead cells. Phagocytosis, endocytotic events sequel to binding particle ligands to the specific receptors on phagocyte cell surface such as Fcgamma recptor (FcgammaR), complement receptor (CR), beta-glucan receptor, and phosphatidylserine (PS) receptor, require actin assembly, pseudopod extension and phagosome closure. Rho GTPases (RhoA, Cdc42, and Rac1) are critically involved in these processes. Abrupt superoxide formation, called as oxidative burst, occurs through NADPH oxidase complex in leukocytes following phagocytosis. NADPH oxidase complex is composed of membrane proteins, p22(PHOX)and gp91(PHOX), and cytosolic proteins, p40(PHOX), p47(PHOX)and p67(PHOX). The cytosolic subunits and Rac-GTP are translocated to the membrane, forming complete NADPH oxidase complex with membrane part subunits. Binding of imunoglobulin G (IgG)- and complement-opsonized particles to FcgammaR and CR of leukocytes induces apoptosis of the cells, which may be due to oxidative burst and accompanying cytochrome c release and casapase-3 activation.
