Granulocyte aggregation as a manifestation of membrane interactions with complement: possible role in leukocyte margination, microvascular occlusion, and endothelial damage.
Activation products of the terminal complement cascade potently affect granulocyte function, inducing, for example, their migration toward (chemotaxis), and adherence to (opsonization), microbes, and stimulating their production of microbicidal oxygen radicals such as superoxide anion, and the like. We present studies that demonstrate that a C5-derived peptide, probably C5a, is a potent promoter of granulocyte and monocyte adhesion to endothelium (margination) and, in addition, causes granulocyte autoaggregation in vitro and in vivo. Although possibly beneficial by producing phagocyte clumps to mechanically entrap unwanted microbes, such aggregates may be deleterious, particularly if sustained, especially in the lung.
D000818:Animals; D001808:Blood Vessels / Q000503:physiopathology*; D002448:Cell Adhesion; D002449:Cell Aggregation; D002462:Cell Membrane / Q000276:immunology; D003182:Complement C5 / Q000276:immunology; D003165:Complement System Proteins / Q000276:immunology*; D004285:Dogs; D004727:Endothelium / Q000503:physiopathology; D006098:Granulocytes / Q000276:immunology*; D006801:Humans; D008168:Lung / Q000503:physiopathology; D051379:Mice; D011817:Rabbits; D006435:Renal Dialysis; D012756:Sheep
D003182:Complement C5; D003165:Complement System Proteins