Microglia in traumatic brain injury

Microglia, which play a major role in the CNS innate immune response, have been increasingly implicated in the acute and chronic neuroinflammatory responses following TBI. Activation of microglia promotes various morphologic changes. Following injury, microglial activation may be detrimental by producing high and sustained levels of pro-inflammatory mediators that may promote neuronal dysfunction and ongoing neurodegeneration. However, microglial activation may be beneficial by clearing unwanted cellular debris, providing anti-inflammatory mediators and neurotrophic factors to promote tissue repair and recovery in the injured brain. The M1-like or pro-inflammatory vs the M2-like or anti-inflammatory polarization classification system has become popular to characterize the heterogeneity of microglial activation following TBI. In this article, we discuss emerging research on microglial activation polarization phenotypes in the context of acute and chronic neuropathologic responses following TBI. Furthermore, we discuss some limitations of the M1-like/M2 polarization scheme and areas for future studies.