Title:Understanding the Multifaceted Role of Inflammatory Mediators in Ischemic Stroke
VOLUME: 21 ISSUE: 18
Author(s):D. Amantea, C. Tassorelli, F. Petrelli, M. Certo, P. Bezzi, G. Micieli, M.T. Corasaniti and G. Bagetta
Affiliation:Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, via Savinio Ed. Polifunzionale, I-87036 Rende (CS), Italy.
Keywords:Brain ischemia, cytokines, immune system, ischemic stroke, neuroinflammation.
Abstract: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.
