The Evolving Landscape of Neuroinflammation After Neonatal Hypoxia-Ischemia
The Evolving Landscape of Neuroinflammation After Neonatal Hypoxia-Ischemia
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DOI：
10.1007/978-3-7091-0693-8_15
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发表时间：
2011-01-01
期刊：
影响因子：
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通讯作者：
Zhang, John H.
中科院分区：
文献类型：
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作者：
Fathali, Nancy;Khatibi, Nikan H.;Zhang, John H.
缺氧缺血性脑损伤仍然是新生儿死亡和发病的主要原因。炎症反应的部分特征是局部免疫细胞的激活，已被认为是缺氧缺血(HI)后未成熟脑损伤进展的核心组成部分。然而，越来越多的证据表明，循环免疫细胞被招募到损伤部位，作为神经元-神经胶质相互作用的协调者和继发性脑损伤的执行者。这表明，将我们的注意力从局部炎症反应转向被认为连接脑-免疫细胞相互作用的分子介质可能是减轻围产期HI炎性后遗症的更有效的方法。在这篇综述中，我们将注意力集中在环氧合酶-2上，这是一种外周免疫细胞可能通过调节大脑中的信号通路而导致预后恶化的介体。此外，我们提出了针对缺氧缺血新生儿神经炎症机制的新的治疗方式的概述。
Hypoxic-ischemic brain injury remains a leading cause of mortality and morbidity in neonates. The inflammatory response, which is characterized in part by activation of local immune cells, has been implicated as a core component for the progression of damage to the immature brain following hypoxia-ischemia (HI). However, mounting evidence implicates circulating immune cells recruited to the site of damage as orchestrators of neuron-glial interactions and perpetuators of secondary brain injury. This suggests that redirecting our attention from the local inflammatory response toward the molecular mediators believed to link brain-immune cell interactions may be a more effective approach to mitigating the inflammatory sequelae of perinatal HI. In this review, we focus our attention on cyclooxygenase-2, a mediator by which peripheral immune cells may modulate signaling pathways in the brain that lead to a worsened outcome. Additionally, we present an overview of emerging therapeutic modalities that target mechanisms of neuroinflammation in the hypoxic-ischemic neonate.