ABSTRACT
A complex pathophysiological mechanism is involved in brain injury following cerebral infarction. The neurovascular unit (NVU) is a complex multi-cellular structure consisting of neurons, endothelial cells, pericyte, astrocyte, microglia and extracellular matrix, etc. The dyshomeostasis of NVU directly participates in the regulation of inflammatory immune process. The components of NVU promote inflammatory overreaction and synergize with the overactivation of autonomic nervous system to initiate stroke-induced immunodepression (SIID). SIID can alleviate the damage caused by inflammation, however, it also makes stroke patients more susceptible to infection, leading to systemic damage. This article reviews the mechanism of SIID and the roles of NVU in SIID, to provide a perspective for reperfusion, prognosis and immunomodulatory therapy of cerebral infarction.
Subject(s)
Humans , Endothelial Cells , Stroke , Neurons/physiology , Immunosuppression Therapy/adverse effects , Cerebral InfarctionABSTRACT
A complex pathophysiological mechanism is involved in the brain injury following cerebral infarction. The neurovascular unit (NVU) is a complex multi-cellular structure consisting of endothelial cells , neurons, glia, smooth muscle cells, and pericytes. The dyshomeostasis of NVU directly participates in the inflammatory immune regulation process. The components of NVU promote inflammatory overreaction and also synergize with the overactivation of autonomic nervous system to initiate stroke-induced immunosuppression (SIID). SIID can alleviate the damage caused by inflammation, however, it also makes stroke patients more susceptible to infection, leading to systemic damage and worsening the condition. This article reviews the mechanism of SIID and the roles of NVU components in SIID, to provide a perspective for recanalization, prognosis and immune regulation therapy of cerebral infarction.