Frontiers in Immunology (Oct 2021)
β2-Adrenergic Receptor Enhances the Alternatively Activated Macrophages and Promotes Biliary Injuries Caused by Helminth Infection
- Stephane Koda,
- Beibei Zhang,
- Beibei Zhang,
- Qian-Yang Zhou,
- 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,
- Xiang-Yang Li,
- Yin-Hai Xu,
- Jia-Xu Chen,
- B. Oneill Telakeng Tekengne,
- Gabriel K. Adzika,
- Ren-Xian Tang,
- Ren-Xian Tang,
- Hong Sun,
- Hong Sun,
- Kui-Yang Zheng,
- Kui-Yang Zheng,
- Chao Yan,
- Chao Yan
Affiliations
- Stephane Koda
- Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Laboratory of Infection and Immunity, Xuzhou Medical University, Xuzhou, China
- Beibei Zhang
- Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Laboratory of Infection and Immunity, Xuzhou Medical University, Xuzhou, China
- Beibei Zhang
- National Demonstration Center for Experimental Basic Medical Science Education, Xuzhou Medical University, Xuzhou, China
- Qian-Yang Zhou
- Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Laboratory of Infection and Immunity, Xuzhou Medical University, Xuzhou, China
- Qian-Yang Zhou
- Department of Dermatology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China
- Na Xu
- Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Laboratory of Infection and Immunity, Xuzhou Medical University, Xuzhou, China
- Jing Li
- Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Laboratory of Infection and Immunity, Xuzhou Medical University, Xuzhou, China
- Ji-Xin Liu
- Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Laboratory of Infection and Immunity, Xuzhou Medical University, Xuzhou, China
- Man Liu
- Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Laboratory of Infection and Immunity, Xuzhou Medical University, Xuzhou, China
- Zi-Yan Lv
- Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Laboratory of Infection and Immunity, Xuzhou Medical University, Xuzhou, China
- Jian-Ling Wang
- Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Laboratory of Infection and Immunity, Xuzhou Medical University, Xuzhou, China
- Yanbiao Shi
- Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Laboratory of Infection and Immunity, Xuzhou Medical University, Xuzhou, China
- Sijia Gao
- Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Laboratory of Infection and Immunity, Xuzhou Medical University, Xuzhou, China
- Qian Yu
- Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Laboratory of Infection and Immunity, Xuzhou Medical University, Xuzhou, China
- Xiang-Yang Li
- Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Laboratory of Infection and Immunity, Xuzhou Medical University, Xuzhou, China
- Xiang-Yang Li
- National Demonstration Center for Experimental Basic Medical Science Education, Xuzhou Medical University, Xuzhou, China
- Yin-Hai Xu
- Department of Laboratory Medicine, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China
- Jia-Xu Chen
- National Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention, Key Laboratory of Parasite and Vector Biology, Ministry of Health, World Health Organization (WHO) Collaborating Center of Malaria, Schistosomiasis, and Filariasis, Shanghai, China
- B. Oneill Telakeng Tekengne
- Department of Clinical Medicine, Xuzhou Medical University, Xuzhou, China
- Gabriel K. Adzika
- Department of Physiology, Xuzhou Medical University, Xuzhou, China
- Ren-Xian Tang
- Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Laboratory of Infection and Immunity, Xuzhou Medical University, Xuzhou, China
- Ren-Xian Tang
- National Demonstration Center for Experimental Basic Medical Science Education, Xuzhou Medical University, Xuzhou, China
- Hong Sun
- National Demonstration Center for Experimental Basic Medical Science Education, Xuzhou Medical University, Xuzhou, China
- Hong Sun
- Department of Physiology, Xuzhou Medical University, Xuzhou, China
- Kui-Yang Zheng
- Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Laboratory of Infection and Immunity, Xuzhou Medical University, Xuzhou, China
- Kui-Yang Zheng
- National Demonstration Center for Experimental Basic Medical Science Education, Xuzhou Medical University, Xuzhou, China
- Chao Yan
- Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Laboratory of Infection and Immunity, Xuzhou Medical University, Xuzhou, China
- Chao Yan
- National Demonstration Center for Experimental Basic Medical Science Education, Xuzhou Medical University, Xuzhou, China
- DOI
- https://doi.org/10.3389/fimmu.2021.754208
- Journal volume & issue
-
Vol. 12
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.
Keywords
