Stroke is a frequent cause of long-term disability and death worldwide. Ischemic stroke is more commonly encountered
compared to hemorrhagic stroke, and leads to tissue death by ischemia due to occlusion of a cerebral artery. Inflammation
is known to result as a result of ischemic injury, long thought to be involved in initiating the recovery and repair
process. However, work over the past few decades indicates that aspects of this inflammatory response may in fact be
detrimental to stroke outcome. Acutely, inflammation appears to have a detrimental effect, and anti-inflammatory treatments
have been been studied as a potential therapeutic target. Chronically, reports suggest that post-ischemic inflammation
is also essential for the tissue repairing and remodeling. The majority of the work in this area has centered around innate
immune mechanisms, which will be the focus of this review. This review describes the different key players in neuroinflammation
and their possible detrimental and protective effects in stroke. A better understanding of the roles of the
different immune cells and their temporal profile of damage versus repair will help to clarify more effective modulation of
inflammation post stroke.
Keywords: Brain ischemia, inflammation, neuroprotection, stroke.
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