Microglial Inflammatory Mechanisms in Stroke: The Jury Is Still Out

Abstract

Microglia represent the main immune cell population in the CNS with unique homeostatic roles and contribution to broad neurological conditions. Stroke is associated with marked changes in microglial phenotypes and induction of inflammatory responses, which emerge as key modulators of brain injury, neurological outcome and regeneration. However, due to the limited availability of functional studies with selective targeting of microglia and microglia-related inflammatory pathways in stroke, the vast majority of observations remain correlative and controversial. Because extensive review articles discussing the role of inflammatory mechanisms in different forms of acute brain injury are available, here we focus on some specific pathways that appear to be important for stroke pathophysiology with assumed contribution by microglia. While the growing toolkit for microglia manipulation increasingly allows targeting inflammatory pathways in a cell-specific manner, reconsideration of some effects devoted to microglia may also be required. This may particularly concern the interpretation of inflammatory mechanisms that emerge in response to stroke as a form of sterile injury and change markedly in chronic inflammation and common stroke comorbidities.