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Updated: May 12, 2026

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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
Ultrasound modulates microglial activity and reduces neuroinflammation in a parameter-dependent manner
Sarina Grewal1,2,3, Francesco Iacoponi4,5, Lok Yin Nicholas Chan1
1Department of Bioengineering, Imperial College London, London, UK.
Summary
Ultrasound therapy can significantly reduce neuroinflammation by lowering pro-inflammatory cytokines like TNF-α, IL-1β, and IL-6. This non-invasive approach shows promise for treating neurological diseases by restoring brain homeostasis.
Area of Science:
- Neuroscience
- Biomedical Engineering
- Immunology
Background:
- Neuroinflammation is a key factor in neurological disease progression.
- Microglia play a central role in neuroinflammation.
- Current treatments for neuroinflammation often have limitations.
Purpose of the Study:
- To investigate the potential of ultrasound to reduce microglia-mediated inflammation.
- To identify optimal ultrasound parameters for anti-inflammatory effects.
- To explore the therapeutic application of ultrasound in neurological conditions.
Main Methods:
- Utilized BV2 microglial cell line stimulated with lipopolysaccharide (LPS).
- Tested various ultrasound parameters (frequency, pressure, duration).
- Assessed pro-inflammatory cytokine levels (TNF-α, IL-1β, IL-6) and NF-κB pathway.
- Validated findings in LPS-treated mice, examining hippocampal TNF-α expression.
Main Results:
- Specific ultrasound parameters significantly reduced pro-inflammatory cytokines in vitro.
- Anti-inflammatory effects persisted for up to 72 hours.
- Ultrasound treatment downregulated the NF-κB pathway.
- In vivo studies showed reduced TNF-α expression in the hippocampus of treated mice.
Conclusions:
- Ultrasound demonstrates potential as a non-invasive therapeutic strategy for neuroinflammation.
- The findings suggest a mechanistic link between ultrasound and the NF-κB pathway.
- Ultrasound may help restore brain homeostasis in neurological diseases.

