BACKGROUND: Airway eosinophilia is a hallmark of aspirin-sensitive asthma/rhinitis. OBJECTIVE: We have investigated chemokine CC-ligand 5 (CCL5) production and its association with eosinophil activation in the upper airways of aspirin-sensitive patients both in vivo and in vitro. METHODS: Twenty aspirin-sensitive asthma/rhinosinusitis patients, 18 atopic-tolerant asthma/rhinosinusitis patients and 15 healthy control subjects took part in the study. All subjects were challenged with saline and lysine-acetylsalicylic acid (L-asa) on separate occasions. Nasal lavages were obtained at baseline and 120 min after challenge and analysed for mediators' release. RESULTS: When compared with control subjects, the baseline levels of CCL5 were significantly increased in both sensitive and tolerant patients (there was no significant difference in CCL5 concentrations between these two groups, P>0.05). However, L-asa nasal challenge induced significantly increased levels of CCL5 in the sensitive patients but not in the tolerant subjects (median: 380 vs. 140 pg/mL, P<0.0001). Similarly, the concentrations of both eosinophil cationic protein (ECP) and cysteinil leukotriene (cys-LTs) were increased significantly in the aspirin-sensitive but not in the tolerant patients. There was a trend towards a significant correlation between CCL5 and ECP concentrations in the sensitive patients following L-ASA challenge. On incubation with aspirin, nasal tissue derived from aspirin-sensitive but not that derived from tolerant subjects released increased CCL5 levels in culture. As determined by immunohistochemistry, CCL5 was predominantly localized to the nasal airway epithelium. CONCLUSION: Altogether, these findings suggest that CCL5 is released in aspirin-sensitive asthma/rhinosinusitis.
BACKGROUND:Airway eosinophilia is a hallmark of aspirin-sensitive asthma/rhinitis. OBJECTIVE: We have investigated chemokine CC-ligand 5 (CCL5) production and its association with eosinophil activation in the upper airways of aspirin-sensitive patients both in vivo and in vitro. METHODS: Twenty aspirin-sensitive asthma/rhinosinusitispatients, 18 atopic-tolerant asthma/rhinosinusitispatients and 15 healthy control subjects took part in the study. All subjects were challenged with saline and lysine-acetylsalicylic acid (L-asa) on separate occasions. Nasal lavages were obtained at baseline and 120 min after challenge and analysed for mediators' release. RESULTS: When compared with control subjects, the baseline levels of CCL5 were significantly increased in both sensitive and tolerant patients (there was no significant difference in CCL5 concentrations between these two groups, P>0.05). However, L-asa nasal challenge induced significantly increased levels of CCL5 in the sensitive patients but not in the tolerant subjects (median: 380 vs. 140 pg/mL, P<0.0001). Similarly, the concentrations of both eosinophil cationic protein (ECP) and cysteinil leukotriene (cys-LTs) were increased significantly in the aspirin-sensitive but not in the tolerant patients. There was a trend towards a significant correlation between CCL5 and ECP concentrations in the sensitive patients following L-ASA challenge. On incubation with aspirin, nasal tissue derived from aspirin-sensitive but not that derived from tolerant subjects released increased CCL5 levels in culture. As determined by immunohistochemistry, CCL5 was predominantly localized to the nasal airway epithelium. CONCLUSION: Altogether, these findings suggest that CCL5 is released in aspirin-sensitive asthma/rhinosinusitis.
Authors: Ma Cristina Negrete-Garcia; Carla Yoneli Jiménez-Torres; Noe Alvarado-Vásquez; A Rosalía Montes-Vizuet; J R Velázquez-Rodriguez; M Carmen Jimenez-Martinez; Luis Manuel Teran-Juárez Journal: ScientificWorldJournal Date: 2012-04-30