Fuentes-Beltrán A, Montes-Vizuet R, Valencia-Maqueda E, Negrete-García M C, García-Cruz M de L, Teran L M
Department of Immunogenetics and Allergy, Instituto Nacional de Enfermedades Respiratorias, Calzada Tlalpan, México.
Clin Exp Allergy. 2009 Apr;39(4):491-9. doi: 10.1111/j.1365-2222.2008.03190.x. Epub 2009 Feb 10.
Airway eosinophilia is a hallmark of aspirin-sensitive asthma/rhinitis.
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.
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.
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.
Altogether, these findings suggest that CCL5 is released in aspirin-sensitive asthma/rhinosinusitis.
气道嗜酸性粒细胞增多是阿司匹林敏感性哮喘/鼻炎的一个标志。
我们在体内和体外研究了趋化因子CC配体5(CCL5)的产生及其与阿司匹林敏感患者上呼吸道嗜酸性粒细胞活化的关系。
20例阿司匹林敏感性哮喘/鼻-鼻窦炎患者、18例特应性耐受哮喘/鼻-鼻窦炎患者和15名健康对照者参与了本研究。所有受试者在不同时间分别接受盐水和赖氨酸-乙酰水杨酸(L-asa)激发。在激发前基线及激发后120分钟采集鼻灌洗液,并分析介质释放情况。
与对照者相比,敏感和耐受患者的CCL5基线水平均显著升高(两组间CCL5浓度无显著差异,P>0.05)。然而,L-asa鼻激发使敏感患者的CCL5水平显著升高,而耐受患者则未升高(中位数:380 vs. 140 pg/mL,P<0.0001)。同样,嗜酸性粒细胞阳离子蛋白(ECP)和半胱氨酰白三烯(cys-LTs)的浓度在阿司匹林敏感患者中显著升高,而在耐受患者中未升高。L-ASA激发后,敏感患者中CCL5与ECP浓度之间存在显著相关趋势。用阿司匹林孵育后,来自阿司匹林敏感患者的鼻组织而非耐受患者的鼻组织在培养中释放的CCL5水平升高。通过免疫组织化学测定,CCL5主要定位于鼻气道上皮。
总之,这些发现表明CCL5在阿司匹林敏感性哮喘/鼻-鼻窦炎中释放。