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

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 knocko...

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Detalles Bibliográficos
Autores principales: 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
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8558246/
https://www.ncbi.nlm.nih.gov/pubmed/34733286
http://dx.doi.org/10.3389/fimmu.2021.754208
Descripción
Sumario: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.