Department of Neurosurgery, Louisiana State University Health Sciences Center, 1501 Kings Highway, Shreveport, LA 71130, USA.
J Leukoc Biol. 2010 May;87(5):779-89. doi: 10.1189/jlb.1109766. Epub 2010 Feb 3.
Inflammation plays an important role in the pathogenesis of ischemic stroke and other forms of ischemic brain injury. Experimentally and clinically, the brain responds to ischemic injury with an acute and prolonged inflammatory process, characterized by rapid activation of resident cells (mainly microglia), production of proinflammatory mediators, and infiltration of various types of inflammatory cells (including neutrophils, different subtypes of T cells, monocyte/macrophages, and other cells) into the ischemic brain tissue. These cellular events collaboratively contribute to ischemic brain injury. Despite intense investigation, there are still numerous controversies concerning the time course of the recruitment of inflammatory cells in the brain and their pathogenic roles in ischemic brain injury. In this review, we provide an overview of the time-dependent recruitment of different inflammatory cells following focal cerebral I/R. We discuss how these cells contribute to ischemic brain injury and highlight certain recent findings and currently unanswered questions about inflammatory cells in the pathophysiology of ischemic stroke.
炎症在缺血性中风和其他形式的缺血性脑损伤的发病机制中起着重要作用。在实验和临床中，大脑对缺血性损伤的反应是一个急性和持久的炎症过程，其特征是常驻细胞（主要是小胶质细胞）的快速激活、促炎介质的产生以及各种类型的炎症细胞（包括中性粒细胞、不同亚型的 T 细胞、单核细胞/巨噬细胞和其他细胞）浸润到缺血性脑组织中。这些细胞事件共同导致缺血性脑损伤。尽管进行了深入的研究，但关于炎症细胞在大脑中的募集时间过程及其在缺血性脑损伤中的致病作用仍存在许多争议。在这篇综述中，我们概述了局灶性脑 I/R 后不同炎症细胞的时间依赖性募集。我们讨论了这些细胞如何导致缺血性脑损伤，并强调了关于缺血性中风病理生理学中炎症细胞的某些最新发现和当前未解决的问题。
