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<p>Macrophages are key regulators of inflammation, capable of adopting pro-inflammatory (M1) or anti-inflammatory (M2) phenotypes in response to environmental cues. In chronic conditions such as post-traumatic osteoarthritis (PTOA), persistent M1 activation contributes to tissue damage and impaired healing. Traditional models using lipopolysaccharide (LPS) to induce inflammation may not fully capture the complex microenvironment of joint injury. This study employs fibronectin fragments (Fnfs), which are associated with matrix degradation, focusing on establishing a physiologically relevant inflammatory model and applying transcriptomic analysis to investigate how <i>continuous low-intensity ultrasound</i> (cLIUS), a non-pharmacological biophysical stimulus, modulates macrophage responses under Fnfs-induced conditions. Beyond identifying differentially expressed genes (DEGs), we introduce <i>differential clustering</i> (DC) to capture transcriptional remodeling, revealing coordinated co-expression shifts overlooked by gene-level analyses. Two modes in the DC analysis, namely same-different (SD) and different-same (DS), capture both canonical and non-canonical M2-associated genes, with only partial overlap between their ranked gene lists, as quantified by concordance indices of 0.52 for SD genes and 0.42 for DS genes (scale 0–1). These findings suggest that cLIUS shifts Fnfs-induced macrophages toward an M2-like reparative phenotype. The coordinated shifts in expression captured by DC complement standard differential expression, providing a perspective on how biophysical treatments such as cLIUS modulate immune cell behavior.</p>

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Continuous low-intensity ultrasound influences the transcriptomic profile in M1 macrophages by downregulating inflammation and promoting M2-like markers

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月14日

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  • Shahid Khan,
  • Owen Trippany,
  • Anuradha Subramanian,
  • Satyaki Roy

摘要

Macrophages are key regulators of inflammation, capable of adopting pro-inflammatory (M1) or anti-inflammatory (M2) phenotypes in response to environmental cues. In chronic conditions such as post-traumatic osteoarthritis (PTOA), persistent M1 activation contributes to tissue damage and impaired healing. Traditional models using lipopolysaccharide (LPS) to induce inflammation may not fully capture the complex microenvironment of joint injury. This study employs fibronectin fragments (Fnfs), which are associated with matrix degradation, focusing on establishing a physiologically relevant inflammatory model and applying transcriptomic analysis to investigate how continuous low-intensity ultrasound (cLIUS), a non-pharmacological biophysical stimulus, modulates macrophage responses under Fnfs-induced conditions. Beyond identifying differentially expressed genes (DEGs), we introduce differential clustering (DC) to capture transcriptional remodeling, revealing coordinated co-expression shifts overlooked by gene-level analyses. Two modes in the DC analysis, namely same-different (SD) and different-same (DS), capture both canonical and non-canonical M2-associated genes, with only partial overlap between their ranked gene lists, as quantified by concordance indices of 0.52 for SD genes and 0.42 for DS genes (scale 0–1). These findings suggest that cLIUS shifts Fnfs-induced macrophages toward an M2-like reparative phenotype. The coordinated shifts in expression captured by DC complement standard differential expression, providing a perspective on how biophysical treatments such as cLIUS modulate immune cell behavior.