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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates

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Aging and peripheral lipopolysaccharide can modulate epigenetic regulators and decrease IL-1β promoter DNA

Stephanie M Matt¹, Marcus A Lawson¹, Rodney W Johnson²

¹Neuroscience Program, University of Illinois at Urbana-Champaign, Urbana, IL, USA; Department of Animal Sciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA.

Neurobiology of Aging

|August 9, 2016

Summary

This summary is machine-generated.

In aged mice, decreased DNA methylation of the interleukin-1 beta (IL-1β) gene promoter leads to heightened microglial activation and prolonged sickness behavior. This suggests DNA methylation regulates neuroinflammation in aging brains.

Keywords:

Aging DNA methylation Interleukin-1 beta Microglia Neuroinflammation

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Area of Science:

Neuroscience
Immunology
Epigenetics

Background:

Aging is associated with exaggerated neuroinflammation and microglial dysfunction following immune stimulation.
Epigenetic modifications, particularly DNA methylation, are implicated in age-related cellular changes.

Purpose of the Study:

To investigate DNA hypomethylation of the interleukin-1 beta (IL-1β) promoter in aged microglia.
To determine if epigenetic changes contribute to microglial dysfunction and neuroinflammation in aging.
To examine the effect of a demethylating agent on IL-1β expression in microglia.

Main Methods:

Analysis of DNA methylation at the IL-1β promoter in microglia from aged and young mice.
Measurement of IL-1β mRNA and protein levels.
Assessment of sickness behavior in response to lipopolysaccharide (LPS).
Treatment of microglial cell lines (BV2) and primary microglia with 5-azacytidine.

Main Results:

Aged mice exhibited decreased IL-1β promoter methylation and increased IL-1β expression in microglia, both basally and after LPS stimulation.
This hypomethylation correlated with increased IL-1β mRNA, intracellular IL-1β, and prolonged sickness behavior.
5-azacytidine treatment induced IL-1β expression and decreased DNA methylation in BV2 and primary microglia, mimicking aged microglia.

Conclusions:

DNA hypomethylation of the IL-1β promoter is a feature of aged microglia.
Epigenetic dysregulation, specifically DNA hypomethylation, contributes to heightened microglial activation and neuroinflammation in the aged brain.
Targeting DNA methylation may offer therapeutic strategies for age-related neuroinflammatory conditions.