Pivotal role of innate myeloid cells in cerebral post-ischemic sterile inflammation
Pivotal role of innate myeloid cells in cerebral post-ischemic sterile inflammation
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DOI：
10.1007/s00281-018-0707-8
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发表时间：
2018-09
影响因子：
9
通讯作者：
Jun Tsuyama;Akari Nakamura;H. Ooboshi;A. Yoshimura;T. Shichita
中科院分区：
文献类型：
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作者：
Jun Tsuyama;Akari Nakamura;H. Ooboshi;A. Yoshimura;T. Shichita
炎症反应在调节缺血性脑损伤后的残疾和恢复中起多方面的作用。在缺血性中风的急性期，驻留的小胶质细胞通过缺血环境引起快速的炎症反应。血脑屏障破坏后，外周来源的中性粒细胞和单核吞噬细胞浸润到缺血脑中。这些浸润的髓样细胞被濒死脑细胞释放的内源性警报分子激活。因此，缺血性中风后的炎症通常由先天免疫触发的无菌炎症组成，其加剧缺血性中风的病理学并影响神经学预后。浸润的免疫细胞维持缺血后炎症数天;然而，在此期间之后，这些细胞承担修复功能，吞噬炎症介质和细胞碎片。缺血性脑中免疫细胞的这种时间特异性极化是一种潜在的新型治疗靶点。在这篇综述中，我们总结了目前的理解的阶段依赖性作用的先天性骨髓细胞在缺血性中风和讨论的细胞和分子机制的炎症或修复极化从治疗的角度来看。
Inflammatory responses play a multifaceted role in regulating both disability and recovery after ischemic brain injury. In the acute phase of ischemic stroke, resident microglia elicit rapid inflammatory responses by the ischemic milieu. After disruption of the blood-brain barrier, peripheral-derived neutrophils and mononuclear phagocytes infiltrate into the ischemic brain. These infiltrating myeloid cells are activated by the endogenous alarming molecules released from dying brain cells. Inflammation after ischemic stroke thus typically consists of sterile inflammation triggered by innate immunity, which exacerbates the pathologies of ischemic stroke and worsens neurological prognosis. Infiltrating immune cells sustain the post-ischemic inflammation for several days; after this period, however, these cells take on a repairing function, phagocytosing inflammatory mediators and cellular debris. This time-specific polarization of immune cells in the ischemic brain is a potential novel therapeutic target. In this review, we summarize the current understanding of the phase-dependent role of innate myeloid cells in ischemic stroke and discuss the cellular and molecular mechanisms of their inflammatory or repairing polarization from a therapeutic perspective.