Inflammation after Ischemic Stroke: The Role of Leukocytes and Glial Cells

Abstract

The immune response after stroke is known to play a major role in ischemic brain pathobiology. The inflammatory signals released by immune mediators activated by brain injury sets off a complex series of biochemical and molecular events which have been increasingly recognized as a key contributor to neuronal cell death. The primary immune mediators involved are glial cells and infiltrating leukocytes, including neutrophils, monocytes and lymphocyte. After ischemic stroke, activation of glial cells and subsequent release of pro- and anti-inflammatory signals are important for modulating both neuronal cell damage and wound healing. Infiltrated leukocytes release inflammatory mediators into the site of the lesion, thereby exacerbating brain injury. This review describes how the roles of glial cells and circulating leukocytes are a double-edged sword for neuroinflammation by focusing on their detrimental and protective effects in ischemic stroke. Here, we will focus on underlying characterize of glial cells and leukocytes under inflammation after ischemic stroke.

Keywords: glial cells; inflammation; ischemic stroke; leukocytes.

Fig. 1. Immune signaling of microglia and astrocyte after ischemic stroke. Resting microglia can be polarized to either the M1 or M2 phenotype. M1 microglia contribute to neuronal damage by pro-inflammatory mediators, whereas M2 microglia improve neuronal protection through anti-inflammatory mediators and phagocytic functions. Astrocytes accumulate at the borders of the lesion, become reactive, and start the formation of a glial scar.