Tsan Any Patricia
نویسنده
چکیده
Phagocytosis of particles by polymorphonuclear leukocytes (PMN) 1 is accompanied by a burst of oxidative metabolic changes. These include increased oxygen consumption (1), hexose monophosphate shunt (HMS) activity (1), and hydrogen peroxide (H202) (2) and superoxide (02-) (3) production. Despite intensive investigation the mechanism by which this oxidative metabolism is stimulated during phagocytosis is still unclear. HMS activity and H20 2 production in resting phagocytes also can be stimulated by a variety of surface-active agents (4, 5), endotoxin (4), phospholipase C (6), concanavalin A (Con A) (7), or leukocyte antibodies in the absence of complement (8). Under these conditions no phagocytosis is necessary, suggesting that mere perturbation of plasma membrane is sufficient for the stimulation of HMS activity and H20 2 production. Recently Goldstein and co-workers provided evidence that the 02generating system is associated with the plasma membrane of PMN (9). Membrane sialic acid has been shown to play a significant role in cell physiology. It is apparently involved in the cell deformability (10). It also plays a dual role in the metabolism of circulating glycoproteins (11). Its presence on liver cell membrane is essential for the binding and transport of serum glycoproteins into the liver cell. In order for binding to occur, however, the glycoprotein must first be desialylated (11). In PMN its presence is necessary for the maximal stimulation of phagocytosis by the natural tetrapeptide, tufl~in (12). In this study, we report the requirement of membrane sialic acid for the stimulation of superoxide production during phagocytosis in human PMN.
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تاریخ انتشار 2003