Intestinal ischemia/reperfusion promotes brain damage via microglia activation: can we do something now?

Microglia are an important immune-mediated communication pathway of the central nervous system and key cellular mediator of neurodegenerative and neuroinflammatory processes. Activation and injury of microglial pathways are associated with a broad range of central nervous system diseases, including brain infection, stroke, and neurodegenerative diseases. When microglia are activated by peripheral inflammation, they produce cytotoxic factors, including tumor necrosis factor-α and interleukin-6, reactive oxygen species, and nitric oxide, resulting in neuronal cell apoptosis accompanied by neurodegeneration. Microglial activation is one of the most common and earliest features of nearly all neuroinflammatory disorders (including stroke, spinal cord injury, encephalitis, multiple sclerosis, Parkinson’s disease, and Alzheimer’s disease). The identification of molecular mechanisms directing microglial function toward pro- or anti-inflammatory functions, as well as in vivo functioning of microglia, is the subject of research and debate. Manipulation of microglial to provide neuroprotection represents a future challenge for neuroscience.