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Ultrasound reduces inflammation by modulating M1/M2 polarization of microglia through STAT1/STAT6/PPARγ signaling
Chin-Hung Hsu1, Yi-Ju Pan2,3, Yin-Ting Zheng1
1Department of Biomedical Imaging and Radiological Sciences, School of Biomedical Science and Engineering, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Introduction:
Activated microglia can be polarized to the pro-inflammatory M1 phenotype and the anti-inflammatory M2 phenotype. Low-intensity pulsed ultrasound (LIPUS) can attenuate pro-inflammatory responses in activated microglia.
Objective:
This study aimed to investigate the effects of LIPUS on M1/M2 polarization of microglial cells and the regulatory mechanisms associated with signaling pathways.
Methods:
BV-2 microglial cells were stimulated by lipopolysaccharide (LPS) to an M1 phenotype or by interleukin-4 (IL-4) to an M2 phenotype. Some microglial cells were exposed to LIPUS, while others were not. M1/M2 marker mRNA and protein expression were measured using real-time polymerase chain reaction and western blot, respectively. Immunofluorescence staining was performed to determine inducible nitric oxide synthase (iNOS)-/arginase-1 (Arg-1)- and CD68-/CD206-positive cells.
Results:
LIPUS treatment significantly attenuated LPS-induced increases in inflammatory markers (iNOS, tumor necrosis factor-α, interleukin-1β, and interleukin-6) as well as the expression of cell surface markers (CD86 and CD68) of M1-polarized microglia. In contrast, LIPUS treatment significantly enhanced the expression of M2-related markers (Arg-1, IL-10, and Ym1) and membrane protein (CD206). LIPUS treatment prevented M1 polarization of microglia and enhanced or sustained M2 polarization by regulating M1/M2 polarization through the signal transducer and activator of transcription 1/STAT6/peroxisome proliferator-activated receptor gamma pathways.
Conclusions:
Our findings suggest that LIPUS inhibits microglial polarization and switches microglia from the M1 to the M2 phenotype.
Insights
Low-intensity pulsed ultrasound (LIPUS) inhibits pro-inflammatory M1 microglia polarization and promotes anti-inflammatory M2 microglia polarization. This study investigated LIPUS effects on microglial polarization and its regulatory mechanisms.
Area of Science:
- Neuroscience
- Immunology
- Biomedical Engineering
Background:
- Microglia play crucial roles in neuroinflammation, with polarization towards M1 (pro-inflammatory) or M2 (anti-inflammatory) phenotypes.
- Activated microglia contribute to various neurological disorders.
- Low-intensity pulsed ultrasound (LIPUS) shows potential in modulating inflammatory responses.
Purpose of the Study:
- To investigate the impact of LIPUS on M1/M2 polarization of microglial cells.
- To elucidate the underlying signaling pathways regulated by LIPUS in microglial polarization.
Main Methods:
- BV-2 microglial cells were polarized to M1 (using lipopolysaccharide) or M2 (using interleukin-4) phenotypes.
- Cells were exposed to LIPUS, and M1/M2 marker expression was analyzed via real-time PCR and western blot.
- Immunofluorescence staining assessed specific M1 and M2 cell surface markers.
Main Results:
- LIPUS significantly reduced M1 markers (e.g., iNOS, CD86, CD68) and pro-inflammatory cytokines (TNF-α, IL-1β, IL-6).
- LIPUS enhanced M2 markers (e.g., Arg-1, IL-10, Ym1, CD206).
- LIPUS modulated M1/M2 polarization via the STAT1/STAT6/PPARγ signaling pathways.
Conclusions:
- LIPUS effectively inhibits microglial M1 polarization.
- LIPUS promotes a shift from the M1 to the M2 microglial phenotype.
- LIPUS represents a potential therapeutic strategy for neuroinflammatory conditions.
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