Lack of association between aspirin triggered 15-hydroxyeicosatetraenoic acid release and mast cell/eosinophil activation in nasal polyps from aspirin-sensitive patients

Background: the mechanism of aspirin sensitivity in patients with asthma and hinosinusitis has been attributed to arachidonic acid metabolism abnormalities. objective: we aimed to test whether aspirin-triggered generation of 15-hydroxyeicosatetraenoic acid (15-hete) in nasal polyp dispersed cells (npdcs) from aspirin-sensitive patients is associated with activation of infl ammatory cells. methods: polyps were obtained from 11 aspirin-sensitive and 19 aspirin-tolerant patients with chronic rhinosinusitis. npdcs were stimulated by aspirin or calcium ionophore. levels of 15-hete,leukotriene (lt) c 4,eosinophil cationic protein (ecp),and tryptase were measured in npdc supernatant. results: npdcs from aspirin-sensitive patients contained more eosinophils (14% vs 9%,p<.05) and released 2.4-fold more ecp (p<.01) at baseline. stimulation with aspirin (200 μm) resulted in a signifi cant increase in 15-hete generation only in tissue from aspirin-sensitive patients (mean increase,82%) but did not induce any increase in the release of ltc 4,ecp,or tryptase. preincubation with calcium ionophore resulted in signifi cantly enhanced generation of 15-hete,ecp,tryptase,and ltc 4 in patients from both groups. incubation of npdcs with misoprostol inhibited aspirin-induced 15-hete generation in aspirin-sensitive patients and calcium ionophore-induced 15-hete,ecp,and tryptase release in both aspirin-sensitive and aspirin-tolerant patients. conclusion: our study demonstrated that aspirin-induced 15-hete generation in nasal polyps from aspirin- ensitive patients is not associated with activation of mast cells and eosinophils. misoprostol has a potent inhibitory effect on the activation of cells derived from the site f nasal mucosal infl ammation,regardless of sensitivity to aspirin. © 2011 esmon publicidad.