| First Author | Koda S | Year | 2021 |
| Journal | Front Immunol | Volume | 12 |
| Pages | 754208 | PubMed ID | 34733286 |
| Mgi Jnum | J:312918 | Mgi Id | MGI:6792193 |
| Doi | 10.3389/fimmu.2021.754208 | Citation | Koda S, et al. (2021) beta2-Adrenergic Receptor Enhances the Alternatively Activated Macrophages and Promotes Biliary Injuries Caused by Helminth Infection. Front Immunol 12:754208 |
| abstractText | 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 beta2-AR deficiency alleviates hepatobiliary damage in mice infected with C. sinensis. Moreover, beta2-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 beta2-AR enhances type 2 immune response through the ERK/mTORC1 signaling pathway in macrophages and their role in liver fibrosis. |
