Understanding the multifaceted role of inflammatory mediators in ischemic stroke

D Amantea, C Tassorelli, F Petrelli, M Certo, P Bezzi, G Micieli, M T Corasaniti, G Bagetta

Research output: Contribution to journalReview articlepeer-review

32 Citations (Scopus)


The evolution of ischemic brain damage is strongly affected by an inflammatory reaction that involves soluble mediators, such as cytokines and chemokines, and specialized cells activated locally or recruited from the periphery. The immune system affects all phases of the ischemic cascade, from the acute intravascular reaction due to blood flow disruption, to the development of brain tissue damage, repair and regeneration. Increased endothelial expression of adhesion molecules and blood-brain barrier breakdown promotes extravasation and brain recruitment of blood-borne cells, including macrophages, neutrophils, dendritic cells and T lymphocytes, as demonstrated both in animal models and in human stroke. Nevertheless, most anti-inflammatory approaches showing promising results in experimental stroke models failed in the clinical setting. The lack of translation may reside in the redundancy of most inflammatory mediators, exerting both detrimental and beneficial functions. Thus, this review is aimed at providing a better understanding of the dualistic role played by each component of the inflammatory/immune response in relation to the spatio-temporal evolution of ischemic stroke injury.

Original languageEnglish
Pages (from-to)2098-117
Number of pages20
JournalCurrent medicinal chemistry
Issue number18
Publication statusPublished - 1 Jan 2014


  • Animals
  • Anti-Inflammatory Agents/therapeutic use
  • Humans
  • Inflammation/immunology
  • Signal Transduction
  • Stroke/drug therapy
  • T-Lymphocytes/immunology
  • Brain ischemia
  • cytokines
  • immune system
  • ischemic stroke
  • neuroinflammation


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