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Interferon Regulatory Factor 5 Mediates Lipopolysaccharide-Induced Neuroinflammation

Ziqi Fan1, Shuai Zhao1, Yueli Zhu1,2

  • 1Department of Neurology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.

Frontiers in Immunology
|December 28, 2020
PubMed
Abstract

Insights

Interferon regulatory factor 5 (IRF5) mediates neuroinflammation in the central nervous system (CNS). Reducing IRF5 levels in mice suppressed inflammatory responses, suggesting IRF5 as a potential therapeutic target for CNS diseases.

Area of Science:

  • Neuroscience
  • Immunology
  • Molecular Biology

Background:

  • Microglia activation drives neuroinflammation, crucial in neurological disease pathogenesis.
  • Interferon regulatory factor 5 (IRF5) is known for peripheral inflammatory roles but its CNS function is unclear.

Purpose of the Study:

  • To investigate the role of IRF5 in lipopolysaccharide (LPS)-induced neuroinflammation in the central nervous system (CNS).
  • To determine if IRF5 could be a therapeutic target for CNS inflammatory conditions.

Main Methods:

  • Neuroinflammation was induced using lipopolysaccharide (LPS) in C57/BL6 mice and BV2 microglial cells.
  • IRF5 expression was down-regulated using siRNA, and its levels were assessed via immunofluorescence and Western blot.
  • Pro-inflammatory cytokine levels (TNF-α, IL-1β, IL-6) were quantified using ELISA and qRT-PCR.

Main Results:

  • LPS significantly increased IRF5 expression in mouse brains, co-localizing with microglia.
  • IRF5 knockdown attenuated LPS-induced increases in TNF-α, IL-1β, and IL-6.
  • Transient neuroinflammation was observed, with IRF5 levels returning to baseline after 24 hours.
  • LPS did not upregulate IRF5 in BV2 microglial cells, indicating IRF5-independent signaling in this model.

Conclusions:

  • IRF5 plays a role in mediating neuroinflammation within the CNS.
  • IRF5 inhibition shows potential for treating CNS inflammatory diseases.
  • LPS-induced inflammation in BV2 microglial cells does not involve IRF5.
Keywords:
IRF5intracerebroventricularlipopolysaccharideneuroinflammationsiRNA interfering

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