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<p>Neuroinflammation contributes to the progression of many neurological diseases. Here, we explore whether ultrasound can reduce microglia-mediated inflammation in vitro and in vivo. We tested a broad range of ultrasound parameters in a BV2 microglial cell line, treated with lipopolysaccharide (LPS) to induce an inflammatory response. We found that specific combinations of centre frequency, acoustic pressure and treatment duration can significantly lower the levels of pro-inflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6. These effects lasted up to 72 h and were associated with the downregulation of the nuclear factor κB (NF-κB), suggesting a mechanistic link between ultrasound and inflammation. Further investigation in vivo, in LPS-treated mice, revealed a reduction in TNF-α expression in the hippocampus following ultrasound. Overall, our findings showcase the potential of ultrasound as a non-invasive therapeutic strategy to reduce neuroinflammation and restore brain homeostasis.</p>

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Ultrasound modulates microglial activity and reduces neuroinflammation in a parameter-dependent manner

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月6日

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  • Sarina Grewal,
  • Francesco Iacoponi,
  • Lok Yin Nicholas Chan,
  • Valeria Dosso,
  • William Lim Kee Chang,
  • Vanessa Drevenakova,
  • Albert Ugwudike,
  • Leonardo Ricotti,
  • Paul M. Matthews,
  • Andrea Cafarelli,
  • Sophie V. Morse

摘要

Neuroinflammation contributes to the progression of many neurological diseases. Here, we explore whether ultrasound can reduce microglia-mediated inflammation in vitro and in vivo. We tested a broad range of ultrasound parameters in a BV2 microglial cell line, treated with lipopolysaccharide (LPS) to induce an inflammatory response. We found that specific combinations of centre frequency, acoustic pressure and treatment duration can significantly lower the levels of pro-inflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6. These effects lasted up to 72 h and were associated with the downregulation of the nuclear factor κB (NF-κB), suggesting a mechanistic link between ultrasound and inflammation. Further investigation in vivo, in LPS-treated mice, revealed a reduction in TNF-α expression in the hippocampus following ultrasound. Overall, our findings showcase the potential of ultrasound as a non-invasive therapeutic strategy to reduce neuroinflammation and restore brain homeostasis.