IJPPP Copyright © 2009-All rights reserved. Published by e-Century Publishing Corporation, Madison, WI 53711
Int J Physiol Pathophysiol Pharmacol 2013;5(2):73-90

Review Article
Microglia and ischemic stroke: a double-edged sword

Anita R Patel, Rodney Ritzel, Louise D McCullough, Fudong Liu

Departments of Neuroscience, Neurology, University of Connecticut Health Center, Farmington, Connecticut 06030

Received April 15, 2013; Accepted May 15, 2013; Epub May 27, 2013; Published June 15, 2013

Abstract: Inflammatory processes have a fundamental role in the pathophysiology of stroke. A key initial event is the rapid activation of
resi-dent immune cells, primarily microglia. This cell population is an important target for new therapeutic approaches to limit stroke
damage. Activation of microglia is normally held in check by strictly controlled mechanisms involving neuronal-glial communication.
Ischemic stroke is a powerful stimulus that disables the endogenous inhibitory signaling and triggers microglial activation. Once
activated, microglia exhibit a spectrum of phenotypes, release both pro- and anti-inflammatory mediators, and function to either
exacerbate ischemic injury or help repair depending on different molecular signals the microglial receptors receive. Various ligands
and receptors have been identified for microglial activation. Experimental tools to detect these inflammatory signals are being
increasingly developed in an effort to define the functional roles of microglia. Fine-tuning immunomodulatory interventions based on the
heterogeneous profiles of microglia are urgently needed for ischemic stroke. (IJPPP1304003).

Keywords: CD45, chimera, inflammatory response, ischemic stroke, macrophage, microglia

Address correspondence to: Dr. Fudong Liu, Department of Neuroscience, University of Connecticut Health Center, 263 Farmington
Ave, Farmington CT, 06030, USA. Phone: 860-679-3508; Fax: 860-679-1181; E-mail: fliu@uchc.edu