Inflammatory mechanisms in ischemic stroke: role of inflammatory cells

Abstract

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.

Figure 1.

Potential inflammatory pathways that respond to cerebral I/R. Mac-1 is a β2-integrin (CD11b/CD18); PSGL-1 actually functions as a ligand for E-/P-/L-selectins.

Figure 2.

Schematic showing a time-dependent recruitment of inflammatory cells into the brain following focal cerebral ischemia in mice. The figure, adapted from (A) ref. [52] and (B) ref. [47] with permission. Note that a transient 60-min MCAO model in C57Bl6 mice was used in both reports.