Department of Anesthesiology, Johns Hopkins University School of Medicine , Baltimore, MD , USA ; Department of Critical Care Medicine, Johns Hopkins University School of Medicine , Baltimore, MD , USA.
Front Pediatr. 2015 Jan 14;2:144. doi: 10.3389/fped.2014.00144. eCollection 2014.
Hypoxic-ischemic (HI) injury to developing brain results from birth asphyxia in neonates and from cardiac arrest in infants and children. It is associated with varying degrees of neurologic sequelae, depending upon the severity and length of HI. Global HI triggers a series of cellular and biochemical pathways that lead to neuronal injury. One of the key cellular pathways of neuronal injury is inflammation. The inflammatory cascade comprises activation and migration of microglia - the so-called "brain macrophages," infiltration of peripheral macrophages into the brain, and release of cytotoxic and proinflammatory cytokines. In this article, we review the inflammatory and immune mechanisms of secondary neuronal injury after global HI injury to developing brain. Specifically, we highlight the current literature on microglial activation in relation to neuronal injury, proinflammatory and anti-inflammatory/restorative pathways, the role of peripheral immune cells, and the potential use of immunomodulators as neuroprotective compounds.
缺氧缺血性（HI）脑损伤是由新生儿出生窒息和婴幼儿心脏骤停引起的。其与神经后遗症的严重程度和持续时间有关。全球 HI 触发了一系列细胞和生化途径，导致神经元损伤。神经元损伤的关键细胞途径之一是炎症。炎症级联反应包括小胶质细胞的激活和迁移-所谓的“脑巨噬细胞”，外周巨噬细胞浸润到大脑中，以及细胞毒性和促炎细胞因子的释放。在本文中，我们综述了全球 HI 损伤发育中脑后的继发性神经元损伤的炎症和免疫机制。具体而言，我们强调了与神经元损伤、促炎和抗炎/修复途径、外周免疫细胞的作用以及免疫调节剂作为神经保护化合物的潜在用途有关的最新文献。
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