INVESTIGADORES
SCHATTNER Mirta Ana
congresos y reuniones científicas
Título:
Aspirin and salicylate prevent polymorphonuclear leukocyte survival mediated by platelets and acidosis.
Autor/es:
MALAVER, E; NEGROTTO, S; PACIENZA, N; D’ATRI, LP; POZNER, RG; URDINEZ, P; GOMEZ, R; SCHATTNER, M
Lugar:
Roma, Italia
Reunión:
Congreso; XIV International Symposium on Atherosclerosis.; 2006
Institución organizadora:
ISA
Resumen:
Objectives:Previous works have demonstrated that platelets (PL) delay polymorphonuclear leukocyte (PMN) apoptosis. Considering that acidosis is a feature of the inflammatory areas, we studied platelet-mediated antiapoptotic effect on PMN cultured in acidic medium. We also examined wether NSAIDs (non-steroidal antiinflammatory drugs) interfere with platelet-mediated prevention of apoptosis. Methods:PMN were obtained from healthy donors and isolated by dextran sedimenation. Platelet-rich plasma was prepared by centrifugation and platelets were washed twice in PBS-prostacyclin-EDTA. PMN and platelets (PMN-PL ratio 1:25) were resuspended in RPMI 1640 supplemented with 2% FBS. Apoptosis was assessed after 18 h by fluorescence microscopy. Results:Extracellular acidosis (pH 6.5) induced a significant inhibition of PMN apoptosis (48 ±6 vs 68 ±4 % apoptosis, p<0.05 n=10). After 36 h culture prevention of PMN apoptosis mediated by either platelets or pH 6.5 was no longer observed (n=3). Pretreatment with aspirin (ASA, 2 mM) and sodium salicylate (NaS, 2mM) at concentrations that per se have no effect on PMN survival, reversed the antiapoptotic effect mediated by acidosis (64 ±5; 64 ±3 n=5) or platelets (59 ±9; 63±9). Indomethacin, a NSAID structurally different from salicylates, had no effect on PMN apoptosis suggesting that ciclooxygenase inhibition is not involved in salicylates action. Conclusions:These results show that while platelets and extracellular acidosis synergize to delay PMN apoptosis, the anti-inflammatory ASA or NaS abrogate these effects. Funding:National Agency of Scientific and Technological Promotion.