Neuroinflammation and M2 microglia: the good, the bad, and the inflamed

Jonathan D Cherry, John A Olschowka, M Kerry O'Banion1

  • 1Department of Neurobiology & Anatomy, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA. Kerry_OBanion@urmc.rochester.edu.

Insights

Microglia, the brain's immune cells, can adopt diverse activation states. This review explores microglial polarization and its therapeutic potential in central nervous system diseases.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • The concept of macrophage activation states is established, with growing interest in resident tissue macrophages like microglia.
  • Peripheral macrophage polarization research does not always directly apply to central nervous system (CNS) microglia.
  • Microglial polarization into distinct states by cytokines is known, but their specific functions remain debated.

Purpose of the Study:

  • To review the various activation states microglia can exhibit.
  • To detail microglial polarization mechanisms and their functional relevance in CNS disease models.
  • To evaluate M2 microglial polarization as a potential therapeutic strategy.

Main Methods:

  • Literature review of microglial polarization studies.
  • Analysis of functional relevance in acute and chronic CNS disease models.
  • Examination of M2 polarization as a therapeutic target.

Main Results:

  • Microglia exhibit multiple polarization states beyond simple pro- or anti-inflammatory roles.
  • Microglial polarization dynamics are crucial in both acute and chronic CNS pathologies.
  • Evidence suggests M2-polarized microglia possess neuroprotective and reparative functions.

Conclusions:

  • Understanding diverse microglial activation states is key to deciphering their role in CNS health and disease.
  • Targeting specific microglial polarization, particularly M2, offers a promising therapeutic avenue for neurological disorders.
  • Further research is needed to fully elucidate functional consequences and optimize M2-based therapies.

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