PDF(Pubmed)
Abstract：
We executed this study to determine if chemerin-like receptor 1 (CMKLR1), a Gi/o protein-coupled receptor expressed by leukocytes and non-leukocytes, contributes to the development of phenotypic features of non-atopic asthma, including airway hyperresponsiveness (AHR) to acetyl-β-methylcholine chloride, lung hyperpermeability, airway epithelial cell desquamation, and lung inflammation. Accordingly, we quantified sequelae of non-atopic asthma in wild-type mice and mice incapable of expressing CMKLR1 (CMKLR1-deficient mice) following cessation of acute inhalation exposure to either filtered room air (air) or ozone (O3), a criteria pollutant and non-atopic asthma stimulus. Following exposure to air, lung elastic recoil and airway responsiveness were greater while the quantity of adiponectin, a multi-functional adipocytokine, in bronchoalveolar lavage (BAL) fluid was lower in CMKLR1-deficient as compared to wild-type mice. Regardless of genotype, exposure to O3 caused AHR, lung hyperpermeability, airway epithelial cell desquamation, and lung inflammation. Nevertheless, except for minimal genotype-related effects on lung hyperpermeability and BAL adiponectin, we observed no other genotype-related differences following O3 exposure. In summary, we demonstrate that CMKLR1 limits the severity of innate airway responsiveness and lung elastic recoil but has a nominal effect on lung pathophysiology induced by acute exposure to O3.
摘要：
我们进行了这项研究，以确定是否chemerin样受体1（CMKLR1），由白细胞和非白细胞表达的Gi/o蛋白偶联受体，有助于非特应性哮喘的表型特征的发展，包括对乙酰-β-甲基胆碱氯化物的气道高反应性（AHR），肺通透性过高,气道上皮细胞脱皮，和肺部炎症。因此，我们在停止急性吸入暴露于过滤的室内空气（空气）或臭氧（O3）后，定量了野生型小鼠和不能表达CMKLR1的小鼠（CMKLR1缺陷小鼠）的非特应性哮喘的后遗症，标准污染物和非特应性哮喘刺激。暴露在空气中之后,肺弹性反冲和气道反应性更大，而脂联素的数量，一种多功能脂肪细胞因子，与野生型小鼠相比，CMKLR1缺陷型小鼠的支气管肺泡灌洗（BAL）液中含量较低。不管基因型如何,暴露于O3导致AHR，肺通透性过高,气道上皮细胞脱皮，和肺部炎症。然而，除了对肺高通透性和BAL脂联素的最小基因型相关影响，我们观察到O3暴露后没有其他基因型相关的差异.总之,我们证明，CMKLR1限制了先天性气道反应性和肺弹性反冲的严重程度，但对急性暴露于O3引起的肺病理生理学具有名义上的影响。
