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

心理压力是哮喘发作的危险因素之一。然而，中枢神经系统感知到的压力与哮喘恶化之间的联系途径仍不清楚。在这个项目中，我们使用我们之前发表的应激性哮喘加重小鼠模型分析了应激相关哮喘加重的机制。我们证明了μ-阿片受体参与中枢神经系统，μ-阿片受体激活后血液中皮质酮水平升高，并进一步扭曲了抗原特异性免疫反应，Th2优势与调节性T细胞发育失败相关。这些发现提示神经-内分泌-免疫轴可能是应激性哮喘加重的一个途径。

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.