caa a22 4500 465763952 CHVBK 20180323111908.0 cr unu---uuuuu 170327e19900201xx s 000 0 eng 10.1007/BF00914026 doi (NATIONALLICENCE)springer-10.1007/BF00914026 Nonsteroidal antiinflammatory drugs exert differential effects on neutrophil function and plasma membrane viscosity [Elektronische Daten] Studies in human neutrophils and liposomes [Steven Abramson, Bruce Cherksey, Delia Gude, Joanna Leszczynska-Piziak, Mark Philips, Lea Blau, Gerald Weissmann] Nonsteroidal antiinflammatory drugs (NSAIDs) inhibit neutrophil functions via mechanisms separate from their capacity to inhibit prostaglandin synthesis. We have studied discrete events in the process of signal transduction: NSAIDs but not a related analgesic drug (acetaminophen), inhibited aggregation in response to the chemoattractants f-Met-Leu-Phe (FMLP), leukotriene B4, and C5a. NSAIDs, but not acetaminophen, inhibited binding of radiolabeled FMLP to purified neutrophil membranes. Gpp(NH)p, a GTPase insensitive analog of GTP, also inhibited the binding of FMLP but, paradoxically, enhanced superoxide anion generation and lysozyme release. The inhibition of ligand binding by NSAIDs did not correlate with their capacity to inhibit FMLP-induced increments in diacylglycerol (DG): piroxicam, but not salicylate effectively inhibited appearance of label ([3H]arachidonate, [14C] glycerol) in DG. Finally, NSAIDs exerted differential effects on the viscosity of neutrophil plasma membranes and multilamellar vesicles (liposomes): membrane viscosity was increased by piroxicam and indomethacin, decreased by salicylate, and unaffected by acetaminophen. Thus, the different effects of NSAIDs on discrete pathways are not due to their shared capacity to reduce ligand binding but rather to a capacity to uncouple postreceptor signaling events that depend upon the state of membrane fluidity. Plenum Publishing Corporation, 1990 Abramson Steven Division of Rheumatology, Department of Medicine, NYU Medical Center, 550 First Avenue, 10016, New York, New York aut Cherksey Bruce Department of Physiology, NYU Medical Center, 550 First Avenue, 10016, New York, New York aut Gude Delia aut Leszczynska-Piziak Joanna aut Philips Mark Division of Rheumatology, Department of Medicine, NYU Medical Center, 550 First Avenue, 10016, New York, New York aut Blau Lea aut Weissmann Gerald Division of Rheumatology, Department of Medicine, NYU Medical Center, 550 First Avenue, 10016, New York, New York aut Inflammation Kluwer Academic Publishers-Plenum Publishers 14/1(1990-02-01), 11-30 0360-3997 14:1<11 1990 14 10753 https://doi.org/10.1007/BF00914026 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00914026 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Abramson Steven Division of Rheumatology, Department of Medicine, NYU Medical Center, 550 First Avenue, 10016, New York, New York aut NATIONALLICENCE 700 1- Cherksey Bruce Department of Physiology, NYU Medical Center, 550 First Avenue, 10016, New York, New York aut NATIONALLICENCE 700 1- Gude Delia aut NATIONALLICENCE 700 1- Leszczynska-Piziak Joanna aut NATIONALLICENCE 700 1- Philips Mark Division of Rheumatology, Department of Medicine, NYU Medical Center, 550 First Avenue, 10016, New York, New York aut NATIONALLICENCE 700 1- Blau Lea aut NATIONALLICENCE 700 1- Weissmann Gerald Division of Rheumatology, Department of Medicine, NYU Medical Center, 550 First Avenue, 10016, New York, New York aut NATIONALLICENCE 773 0- Inflammation Kluwer Academic Publishers-Plenum Publishers 14/1(1990-02-01), 11-30 0360-3997 14:1<11 1990 14 10753 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer