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Early P2X7R-dependent activation of microglia during the asymptomatic phase of autoimmune encephalomyelitis

Tomasz Grygorowicz1, Lidia Strużyńska2

  • 1Laboratory of Pathoneurochemistry, Department of Neurochemistry, Mossakowski Medical Research Centre, Polish Academy of Sciences, 5 Pawińskiego str., 02-106, Warsaw, Poland.

Inflammopharmacology
|September 14, 2018
PubMed

Insights

Microglia activation and neuroinflammation occur early in experimental autoimmune encephalomyelitis (EAE), the animal model for multiple sclerosis (MS). Blocking the P2X7 receptor reduces this early inflammation and delays disease symptoms.

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Microglia-mediated neuroinflammation is central to central nervous system (CNS) diseases like multiple sclerosis (MS).
  • The purinergic P2X7 receptor (P2X7R) plays a critical role in this inflammatory response.
  • While microgliosis is known in advanced MS, its role in early disease stages is less understood.

Purpose of the Study:

  • To investigate the temporal dynamics of microglial activation in the early stages of experimental autoimmune encephalomyelitis (EAE), an animal model for MS.
  • To examine the role of the purinergic P2X7 receptor (P2X7R) in early microglial activation and neuroinflammation during EAE.
  • To evaluate the therapeutic potential of P2X7R antagonism in mitigating EAE progression.

Main Methods:

  • Induction of EAE in rats as an animal model for MS.
  • Assessment of microglial activation using Iba-1 immunoreactivity and morphological analysis at various time points post-immunization.
  • Measurement of P2X7R expression in microglia.
  • Administration of Brilliant Blue G, a P2X7R antagonist, to assess its effects on disease onset, neurological symptoms, and neuroinflammation.
  • Quantification of proinflammatory cytokines (IL-1β, IL-6, TNF-α) in brain tissue.

Main Results:

  • Microglial activation, indicated by increased Iba-1 immunoreactivity and morphological changes, was observed as early as day 4 post-immunization, preceding neurological symptom development.
  • P2X7R expression was concurrently upregulated in activated microglia.
  • Treatment with Brilliant Blue G delayed EAE onset, partially ameliorated neurological deficits, and significantly reduced microglial activation and neuroinflammation.
  • P2X7R blockade led to decreased levels of IL-1β, IL-6, and TNF-α in the EAE rat brains.

Conclusions:

  • Microglia are activated and contribute to neuroinflammation at a very early stage of EAE/MS.
  • This early neuroinflammation is dependent on the purinergic P2X7 receptor (P2X7R) pathway.
  • Targeting P2X7R represents a potential therapeutic strategy to intervene in the early inflammatory processes of MS.
Keywords:
Brilliant Blue GEAEIba-1Multiple sclerosisNeuroinflammationPurinergic receptors

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