β2-Adrenergic Receptor Enhances the Alternatively Activated Macrophages and Promotes Biliary Injuries Caused by Helminth Infection.

Frontiers in immunology 2021

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The autonomic nervous system has been studied for its involvement in the control of macrophages; however, the mechanisms underlying the interaction between the adrenergic receptors and alternatively activated macrophages (M2) remain obscure. Using FVB wild-type and beta 2 adrenergic receptors knockout, we found that β2-AR deficiency alleviates hepatobiliary damage in mice infected with C. sinensis. Moreover, β2-AR-deficient mice decrease the activation and infiltration of M2 macrophages and decrease the production of type 2 cytokines, which are associated with a significant decrease in liver fibrosis in infected mice. Our in vitro results on bone marrow-derived macrophages revealed that macrophages from Adrb2-/- mice significantly decrease M2 markers and the phosphorylation of ERK/mTORC1 induced by IL-4 compared to that observed in M2 macrophages from Adrb2+/+ . This study provides a better understanding of the mechanisms by which the β2-AR enhances type 2 immune response through the ERK/mTORC1 signaling pathway in macrophages and their role in liver fibrosis. Copyright © 2021 Koda, Zhang, Zhou, Xu, Li, Liu, Liu, Lv, Wang, Shi, Gao, Yu, Li, Xu, Chen, Tekengne, Adzika, Tang, Sun, Zheng and Yan.

Citation

Stephane Koda, Beibei Zhang, Qian-Yang Zhou, Na Xu, Jing Li, Ji-Xin Liu, Man Liu, Zi-Yan Lv, Jian-Ling Wang, Yanbiao Shi, Sijia Gao, Qian Yu, Xiang-Yang Li, Yin-Hai Xu, Jia-Xu Chen, B Oneill Telakeng Tekengne, Gabriel K Adzika, Ren-Xian Tang, Hong Sun, Kui-Yang Zheng, Chao Yan. β2-Adrenergic Receptor Enhances the Alternatively Activated Macrophages and Promotes Biliary Injuries Caused by Helminth Infection. Frontiers in immunology. 2021;12:754208