The role of opioid receptors-allergic immune responses axis in stress-induced asthma

心理应激是哮喘急性发作的危险因素之一。然而，将中枢神经系统中感知到的压力与哮喘急性发作联系起来的途径仍然不清楚。在这个项目中，我们使用我们先前发表的应激诱发哮喘急性发作的小鼠模型分析了应激相关哮喘急性发作的潜在机制。我们证实了中枢神经系统中μ-阿片受体的参与，以及应激相关哮喘急性发作中μ-阿片受体激活后血液中皮质酮水平的增加，以及与调节性T细胞发育失败相关的Th 2优势抗原特异性免疫应答的进一步偏斜。这些发现表明神经内分泌免疫轴作为一个可能的途径，在应激诱导的哮喘急性发作。

Psychological stress has been well characterized as one of risk factors for asthma exacerbations. However, pathways linking the stress perceived in the central nervous system to asthma exacerbations still remain unclear. In this project, we analyzed mechanisms underlying stress-related asthma exacerbations using a murine model of stress-induced asthma exacerbations that we previously published. We demonstrated the involvement of μ-opioid receptors in the central nervous system and the increase of corticosterone levels in blood following the activation of the μ-opioid receptors in stress-related asthma exacerbations, and further skewing of antigen-specific immune responses to Th2 predominance associated with the failure of regulatory T cell development. These findings suggest the neuro-endocrino-immune axis as a possible pathway in stress-induced asthma exacerbations.