Control of Neuroinflammation through Radiation-Induced Microglial Changes

Cells. 2021 Sep 10;10(9):2381. doi: 10.3390/cells10092381.

Abstract

Microglia, the innate immune cells of the central nervous system, play a pivotal role in the modulation of neuroinflammation. Neuroinflammation has been implicated in many diseases of the CNS, including Alzheimer's disease and Parkinson's disease. It is well documented that microglial activation, initiated by a variety of stressors, can trigger a potentially destructive neuroinflammatory response via the release of pro-inflammatory molecules, and reactive oxygen and nitrogen species. However, the potential anti-inflammatory and neuroprotective effects that microglia are also thought to exhibit have been under-investigated. The application of ionising radiation at different doses and dose schedules may reveal novel methods for the control of microglial response to stressors, potentially highlighting avenues for treatment of neuroinflammation associated CNS disorders, such as Alzheimer's disease and Parkinson's disease. There remains a need to characterise the response of microglia to radiation, particularly low dose ionising radiation.

Keywords: TSPO; antioxidants; cytokines; microglia; mitochondria; neuroinflammation.

Publication types

  • Review

MeSH terms

  • Animals
  • Dose-Response Relationship, Radiation
  • Humans
  • Immunity, Innate / radiation effects
  • Inflammation Mediators / metabolism*
  • Microglia / immunology
  • Microglia / metabolism
  • Microglia / pathology
  • Microglia / radiation effects*
  • Neurodegenerative Diseases / immunology
  • Neurodegenerative Diseases / metabolism
  • Neurodegenerative Diseases / pathology
  • Neurodegenerative Diseases / radiotherapy*
  • Neuroimmunomodulation / radiation effects*
  • Nitrosative Stress / radiation effects
  • Oxidative Stress / radiation effects
  • Phenotype
  • Reactive Nitrogen Species / metabolism*
  • Reactive Oxygen Species / metabolism*
  • Receptors, GABA / metabolism

Substances

  • Inflammation Mediators
  • Reactive Nitrogen Species
  • Reactive Oxygen Species
  • Receptors, GABA
  • TSPO protein, human