About this Journal Submit a Manuscript Table of Contents
Clinical and Developmental Immunology
Volume 2013 (2013), Article ID 746068, 10 pages
http://dx.doi.org/10.1155/2013/746068
Review Article

Microglial Responses after Ischemic Stroke and Intracerebral Hemorrhage

1Department of Immunology, University of Connecticut Health Center, Farmington, CT 06032, USA
2Department of Neuroscience, University of Connecticut Health Center, Farmington, CT 06032, USA
3Department of Neurology, University of Connecticut Health Center and Hartford Hospital, Hartford, CT 06102, USA
4Department of Neurosurgery, Hartford Hospital, Hartford, CT 06102, USA

Received 10 May 2013; Revised 6 August 2013; Accepted 28 August 2013

Academic Editor: Jeffrey Zirger

Copyright © 2013 Roslyn A. Taylor and Lauren H. Sansing. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Stroke is a leading cause of death worldwide. Ischemic stroke is caused by blockage of blood vessels in the brain leading to tissue death, while intracerebral hemorrhage (ICH) occurs when a blood vessel ruptures, exposing the brain to blood components. Both are associated with glial toxicity and neuroinflammation. Microglia, as the resident immune cells of the central nervous system (CNS), continually sample the environment for signs of injury and infection. Under homeostatic conditions, they have a ramified morphology and phagocytose debris. After stroke, microglia become activated, obtain an amoeboid morphology, and release inflammatory cytokines (the M1 phenotype). However, microglia can also be alternatively activated, performing crucial roles in limiting inflammation and phagocytosing tissue debris (the M2 phenotype). In rodent models, microglial activation occurs very early after stroke and ICH; however, their specific roles in injury and repair remain unclear. This review summarizes the literature on microglial responses after ischemic stroke and ICH, highlighting the mediators of microglial activation and potential therapeutic targets for each condition.