1. M1-type polarized macrophage contributes to brain damage through CXCR3.2/CXCL11 pathways after RGNNV infection in grouper.
- Author
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Liang K, Zhang M, Liang J, Zuo X, Jia X, Shan J, Li Z, Yu J, Xuan Z, Luo L, Zhao H, Gan S, Liu D, Qin Q, and Wang Q
- Subjects
- Animals, Chemokine CXCL11, Receptors, CXCR3 metabolism, Bass immunology, Bass virology, Signal Transduction, Cytokines metabolism, Cytokines immunology, Fish Proteins immunology, Fish Proteins genetics, Macrophages immunology, Macrophages virology, Fish Diseases virology, Fish Diseases immunology, Brain virology, Brain immunology, Brain pathology, Nodaviridae physiology, RNA Virus Infections immunology, RNA Virus Infections virology
- Abstract
The vertebrate central nervous system (CNS) is the most complex system of the body. The CNS, especially the brain, is generally regarded as immune-privileged. However, the specialized immune strategies in the brain and how immune cells, specifically macrophages in the brain, respond to virus invasion remain poorly understood. Therefore, this study aimed to examine the potential immune response of macrophages in the brain of orange-spotted groupers ( Epinephelus coioides ) following red-spotted grouper nervous necrosis virus (RGNNV) infection. We observed that RGNNV induced macrophages to produce an inflammatory response in the brain of orange-spotted grouper, and the macrophages exhibited M1-type polarization after RGNNV infection. In addition, we found RGNNV-induced macrophage M1 polarization via the CXCR3.2- CXCL11 pathway. Furthermore, we observed that RGNNV triggered M1 polarization in macrophages, resulting in substantial proinflammatory cytokine production and subsequent damage to brain tissue. These findings reveal a unique mechanism for brain macrophage polarization, emphasizing their role in contributing to nervous tissue damage following viral infection in the CNS.
- Published
- 2024
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