Inflammatory responses in hypoxic ischemic encephalopathy

Abstract

Inflammation plays a critical role in mediating brain injury induced by neonatal hypoxic ischemic encephalopathy (HIE). The mechanisms underlying inflammatory responses to ischemia may be shared by neonatal and adult brains; however, HIE exhibits a unique inflammation phenotype that results from the immaturity of the neonatal immune system. This review will discuss the current knowledge concerning systemic and local inflammatory responses in the acute and subacute stages of HIE. The key components of inflammation, including immune cells, adhesion molecules, cytokines, chemokines and oxidative stress, will be reviewed, and the differences between neonatal and adult inflammatory responses to cerebral ischemic injury will also be discussed.

Figure 1

Schematic diagram of inflammatory responses in ischemic stroke. When stroke occurs, microglia are activated and develop macrophage-like capabilities including phagocytosis, cytokine and chemokine production, antigen presentation and the release of MMPs that weaken the BBB. As a result, peripheral leukocytes infiltrate into the brain, leading to exacerbation of inflammation and neuronal injury. MG, microglia; MP, macrophage; NE, neuron; NP, neutrophil; LC, lymphocyte; MN, monocyte; EC, erythrocyte.