AUTHOR=Koda Stephane , Zhang Beibei , Zhou Qian-Yang , Xu Na , Li Jing , Liu Ji-Xin , Liu Man , Lv Zi-Yan , Wang Jian-Ling , Shi Yanbiao , Gao Sijia , Yu Qian , Li Xiang-Yang , Xu Yin-Hai , Chen Jia-Xu , Tekengne B. Oneill Telakeng , Adzika Gabriel K. , Tang Ren-Xian , Sun Hong , Zheng Kui-Yang , Yan Chao TITLE=β2-Adrenergic Receptor Enhances the Alternatively Activated Macrophages and Promotes Biliary Injuries Caused by Helminth Infection JOURNAL=Frontiers in Immunology VOLUME=12 YEAR=2021 URL=https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2021.754208 DOI=10.3389/fimmu.2021.754208 ISSN=1664-3224 ABSTRACT=

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.