Inflammatory mechanisms after ischemia and stroke

Research output: Contribution to journalReview articlepeer-review

480 Scopus citations


Inflammation has been implicated as a secondary injury mechanism following ischemia and stroke. A variety of experimental models, including thromboembolic stroke, focal and global ischemia, have been used to evaluate the importance of inflammation. The vasculature endothelium promotes inflammation through the upregulation of adhesion molecules such as ICAM, E-selectin, and P-selectin that bind to circulating leukocytes and facilitate their migration into the CNS. Once in the CNS, the production of cytotoxic molecules may facilitate cell death. The macrophage and microglial response to injury may either be beneficial by scavenging necrotic debris or detrimental by facilitating cell death in neurons that would otherwise recover. While many studies have tested these hypotheses, the importance of inflammation in these models is inconclusive. This review summarizes data regarding the role of the vasculature, leukocytes, blood-brain barrier, macrophages, and microglia after experimental and clinical stroke.

Original languageEnglish (US)
Pages (from-to)127-136
Number of pages10
JournalJournal of neuropathology and experimental neurology
Issue number2
StatePublished - Feb 1 2003


  • Adhesion molecules
  • Blood-brain barrier
  • Inflammation
  • Ischemia
  • Microglia
  • Stroke

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Neuroscience(all)


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