小胶质细胞
神经炎症
炎症
神经病理性疼痛
神经科学
巨噬细胞
医学
巨噬细胞极化
慢性疼痛
免疫学
生物
生物化学
体外
作者
Ouyang Chen,Xin Luo,Ru-Rong Ji
出处
期刊:Medical review
[De Gruyter]
日期:2023-10-01
卷期号:3 (5): 381-407
摘要
Abstract Pain is a main symptom in inflammation, and inflammation induces pain via inflammatory mediators acting on nociceptive neurons. Macrophages and microglia are distinct cell types, representing immune cells and glial cells, respectively, but they share similar roles in pain regulation. Macrophages are key regulators of inflammation and pain. Macrophage polarization plays different roles in inducing and resolving pain. Notably, macrophage polarization and phagocytosis can be induced by specialized pro-resolution mediators (SPMs). SPMs also potently inhibit inflammatory and neuropathic pain via immunomodulation and neuromodulation. In this review, we discuss macrophage signaling involved in pain induction and resolution, as well as in maintaining physiological pain. Microglia are macrophage-like cells in the central nervous system (CNS) and drive neuroinflammation and pathological pain in various inflammatory and neurological disorders. Microglia-produced inflammatory cytokines can potently regulate excitatory and inhibitory synaptic transmission as neuromodulators. We also highlight sex differences in macrophage and microglial signaling in inflammatory and neuropathic pain. Thus, targeting macrophage and microglial signaling in distinct locations via pharmacological approaches, including immunotherapies, and non-pharmacological approaches will help to control chronic inflammation and chronic pain.
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