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, p22PHOX and gp91PHOX, and cytosolic proteins, p40PHOX, p47PHOX and p67PHOX. 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.
Highlights
In this review, a series of phagocytosis, superoxide formation and apoptosis of phagocyte cells will be discussed
LIM kinase-1 (LIMK1) regulates the macrophage-like U937 cells through phosphorylation of cofilin and enhances the formation of filamentous actin. This results lead to the increase of phagocytosis, superoxide production, and translocation of LIMK1 to plasma membrane, when the cells are activated with opsonized zymosan particles (Matsui et al, 2002)
Subsequent to phagocytosis in macrophage, there is an abrupt increase of superoxide formation known as the oxidative burst, which is catalyzed by an NADPH oxidase enzyme complex
Summary
Abbreviations: FcR, Fc receptor; CR, complement receptor; fMLP, formyl-methionyl-leucyl-phenylalanine; GAP, GTPase-activating protein; GEF, guanine nucleotide exchange factor; GM-CSF, granulocyte macrophage colony-stimulating factor; GXM, glucuronoxylmannan; IOZ, IgG-opsonized zymosan; COZ, complementopsonized zymosan; IFN-γ, interferon-γ; IgG, imunoglobulin G; ITAMs, immunoglobulin gene family tyrosine activation motifs; JNK, c-jun N-terminal kinase; LIMK, LIM kinase; LPS, lipopolysaccharide; MLCK, myosin light chain kinase; NO, nitric oxide; NSF, N-ethylmaleimide-sensitive factor; OPMN, PMN in the oral cavity; PAF, platelet activating factor; PH, pleckstrin homology; PMA, phorbol 12-myristate 13-acetate; PKC, protein kinase C; PAK, p21-activated kinase; PI3K, phosphatidylinositol-3 kinase; PIP3, phosphatidylinositol-3,4,5-triphosphate; PLD, phospholipase D; PMN, polymorphonuclear leukocytes; PS, phosphatidylserine; SHIP, src homology 2 domain-containing inositol 5'-phosphatase; RhoGDI, Rho GDP dissociation inhibitor; ROK, Rho-dependent protein kinase; ROS, reactive oxygen species, TNFR, tumor necrosis factor receptor; SAPK, stress activating protein kinase; SH2, Src homology 2; SNARE, soluble NSF attachment protein receptor; TNF-α, tumor necorsis factor-α; VAMP, Vesicle-associated membrane protein; WASP, Wiskott-Aldrich syndrome protein
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