吸入性腺苷A2A受体激动剂对变应原诱导的迟发性哮喘反应的影响。
Effect of an inhaled adenosine A2A agonist on the allergen-induced late asthmatic response.
作者信息
Luijk B, van den Berge M, Kerstjens H A M, Postma D S, Cass L, Sabin A, Lammers J-W J
机构信息
Department of Pulmonary Diseases, Heart Lung Center Utrecht, University Medical Center Utrecht, Utrecht, The Netherlands.
出版信息
Allergy. 2008 Jan;63(1):75-80. doi: 10.1111/j.1398-9995.2007.01557.x. Epub 2007 Oct 18.
BACKGROUND
Adenosine receptor activation is suggested to play a role in asthmatic airway inflammation. Inhibition of adenosine receptors may have an effect on the late asthmatic response (LAR) after allergen inhalation and this mechanism could offer a potential new treatment in asthma.
METHODS
We evaluated the effect of an inhaled adenosine-(2A) (A(2A))-receptor agonist (GW328267X), 25 microg, in 15 nonsmoking atopic asthmatics who underwent an inhaled allergen challenge following twice daily treatment for 1 week in a double-blind, placebo- and fluticasone propionate (250 microg) controlled study.
RESULTS
In contrast to fluticasone, treatment with the A(2A)-receptor agonist neither significantly protect against the allergen-induced early and late asthmatic reaction, nor the accompanying inflammatory response as measured by sputum total cell counts, number of EG2+ cells, and the concentration of interleukin-8 and eosinophil cationic protein.
CONCLUSION
The inhaled A(2A)-receptor agonist, GW328267X, 25 microg does not affect the allergen-induced LAR or the associated inflammatory response in asthma.
背景
腺苷受体激活被认为在哮喘气道炎症中起作用。抑制腺苷受体可能对吸入变应原后的哮喘迟发反应（LAR）产生影响，并且这种机制可能为哮喘提供一种潜在的新治疗方法。
方法
我们评估了吸入25微克腺苷A2A受体激动剂（GW328267X）对15名不吸烟的特应性哮喘患者的影响，这些患者在一项双盲、安慰剂和丙酸氟替卡松（250微克）对照研究中，接受每日两次治疗1周后进行吸入变应原激发试验。
结果
与氟替卡松相反，A2A受体激动剂治疗既不能显著预防变应原诱导的早期和迟发性哮喘反应，也不能预防伴随的炎症反应，炎症反应通过痰液总细胞计数、EG2 +细胞数量以及白细胞介素-8和嗜酸性粒细胞阳离子蛋白浓度来衡量。
结论
吸入25微克的A2A受体激动剂GW328267X不影响变应原诱导的哮喘LAR或相关的炎症反应。
Zotero 插件