State Key Laboratory for Animal Disease Control and Prevention, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin 150069, China.
College of Veterinary Medicine, Shanxi Agricultural University, Taigu, Jinzhong 030801, China.
Int J Mol Sci. 2024 Nov 10;25(22):12078. doi: 10.3390/ijms252212078.
Numerous viruses that propagate through the respiratory tract may be initially engulfed by macrophages (Ms) within the alveoli, where they complete their first replication cycle and subsequently infect the adjacent epithelial cells. This process can lead to significant pathological damage to tissues and organs, leading to various diseases. As essential components in host antiviral immune systems, Ms can be polarized into pro-inflammatory M1 Ms or anti-inflammatory M2 Ms, a process involving multiple signaling pathways and molecular mechanisms that yield diverse phenotypic and functional features in response to various stimuli. In general, when infected by a virus, M1 macrophages secrete pro-inflammatory cytokines to play an antiviral role, while M2 macrophages play an anti-inflammatory role to promote the replication of the virus. However, recent studies have shown that some viruses may exhibit the opposite trend. Viruses have evolved various strategies to disrupt M polarization for efficient replication and transmission. Notably, various factors, such as mechanical softness, the altered pH value of the endolysosomal system, and the homeostasis between M1/M2 Ms populations, contribute to crucial events in the viral replication cycle. Here, we summarize the regulation of M polarization, virus-induced alterations in M polarization, and the antiviral mechanisms associated with these changes. Collectively, this review provides insights into recent advances regarding M polarization in host antiviral immune responses, which will contribute to the development of precise prevention strategies as well as management approaches to disease incidence and transmission.
许多通过呼吸道传播的病毒可能最初被肺泡中的巨噬细胞（Ms）吞噬，在那里它们完成第一个复制周期，然后感染相邻的上皮细胞。这个过程可能导致组织和器官的重大病理损伤，导致各种疾病。作为宿主抗病毒免疫系统的重要组成部分，Ms 可以极化成为促炎的 M1 Ms 或抗炎的 M2 Ms，这个过程涉及多个信号通路和分子机制，根据不同的刺激产生不同的表型和功能特征。一般来说，当被病毒感染时，M1 巨噬细胞会分泌促炎细胞因子来发挥抗病毒作用，而 M2 巨噬细胞则发挥抗炎作用来促进病毒的复制。然而，最近的研究表明，一些病毒可能表现出相反的趋势。病毒已经进化出各种策略来破坏 M 极化以实现有效的复制和传播。值得注意的是，各种因素，如机械柔软度、内溶酶体系统 pH 值的改变以及 M1/M2 Ms 群体之间的平衡，都有助于病毒复制周期中的关键事件。在这里，我们总结了 M 极化的调节、病毒诱导的 M 极化改变以及与这些变化相关的抗病毒机制。总之，这篇综述提供了对宿主抗病毒免疫反应中 M 极化的最新进展的见解，这将有助于制定精确的预防策略以及对疾病发生和传播的管理方法。
