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

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

  • Front Immunol. 2021 Oct 18:12:754208. doi: 10.3389/fimmu.2021.754208.
Stephane Koda 1,  Beibei Zhang 1 2,  Qian-Yang Zhou 1 3,  Na Xu 1,  Jing Li 1,  Ji-Xin Liu 1,  Man Liu 1,  Zi-Yan Lv 1,  Jian-Ling Wang 1,  Yanbiao Shi 1,  Sijia Gao 1,  Qian Yu 1,  Xiang-Yang Li 1 2,  Yin-Hai Xu 4,  Jia-Xu Chen 5,  B Oneill Telakeng Tekengne 6,  Gabriel K Adzika 7,  Ren-Xian Tang 1 2,  Hong Sun 2 7,  Kui-Yang Zheng 1 2,  Chao Yan 1 2
Affiliations

Affiliations

  • 1 Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Laboratory of Infection and Immunity, Xuzhou Medical University, Xuzhou, China.
  • 2 National Demonstration Center for Experimental Basic Medical Science Education, Xuzhou Medical University, Xuzhou, China.
  • 3 Department of Dermatology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
  • 4 Department of Laboratory Medicine, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China.
  • 5 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.
  • 6 Department of Clinical Medicine, Xuzhou Medical University, Xuzhou, China.
  • 7 Department of Physiology, Xuzhou Medical University, Xuzhou, China.
PMID: 34733286 DOI: 10.3389/fimmu.2021.754208
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

Clonorchis sinensis; ERK/mTORC1 signaling; beta 2 adrenergic receptor; liver fibrosis; macrophages.

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