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<p>Chronic inflammation is the underlying cause of the pathogenesis of many critical diseases. Therapeutic interventions for controlling inflammation via targeted gene knockdown of inflammatory mediators have emerged as a promising approach for regulating uncontrolled inflammation. This study explores the potential of siIL-1β-anti-CD44-Liposomes (SIL) as a potent anti-inflammatory therapy via gene-specific knockdown of <i>IL-1β</i> mRNA through CD44-targeted Immunoliposomes. The designed SIL exhibited a uniform size of 131.1 ± 0.5 nm with a quasi-spherical morphology and sustained release of siIL-1β within 24 hours. The efficacy of SIL in rendering anti-inflammatory effects was validated on cellular as well as preclinical models of inflammation. SIL treatment resulted in a significant reduction of <i>IL-1β</i> and <i>TNF-α</i> at both gene and protein expression levels, alongside down-regulation of additional pro-inflammatory markers, coupled with an increase in the anti-inflammatory cytokine IL-4. Furthermore, SIL modulated macrophage-T cell crosstalk, attenuating cytokine-driven T cell effector responses. In the preclinical model of inflammation, SIL demonstrated robust anti-inflammatory activity reflected by decreased systemic inflammatory markers such as C-reactive protein, and by broad immunomodulatory effects at the tissue and cytokine levels. Collectively, these findings underscore the therapeutic potential of siIL-1β-anti-CD44-liposomes as a targeted and multifaceted intervention for chronic inflammatory disorders.</p><p></p>

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CD44-targeted immunoliposomes for IL-1β knockdown modulate macrophage-mediated inflammation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月13日

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  • Haly Shukla,
  • Simran Nasra,
  • Milonee Patel,
  • Dhiraj Bhatia,
  • Ashutosh Kumar

摘要

Chronic inflammation is the underlying cause of the pathogenesis of many critical diseases. Therapeutic interventions for controlling inflammation via targeted gene knockdown of inflammatory mediators have emerged as a promising approach for regulating uncontrolled inflammation. This study explores the potential of siIL-1β-anti-CD44-Liposomes (SIL) as a potent anti-inflammatory therapy via gene-specific knockdown of IL-1β mRNA through CD44-targeted Immunoliposomes. The designed SIL exhibited a uniform size of 131.1 ± 0.5 nm with a quasi-spherical morphology and sustained release of siIL-1β within 24 hours. The efficacy of SIL in rendering anti-inflammatory effects was validated on cellular as well as preclinical models of inflammation. SIL treatment resulted in a significant reduction of IL-1β and TNF-α at both gene and protein expression levels, alongside down-regulation of additional pro-inflammatory markers, coupled with an increase in the anti-inflammatory cytokine IL-4. Furthermore, SIL modulated macrophage-T cell crosstalk, attenuating cytokine-driven T cell effector responses. In the preclinical model of inflammation, SIL demonstrated robust anti-inflammatory activity reflected by decreased systemic inflammatory markers such as C-reactive protein, and by broad immunomodulatory effects at the tissue and cytokine levels. Collectively, these findings underscore the therapeutic potential of siIL-1β-anti-CD44-liposomes as a targeted and multifaceted intervention for chronic inflammatory disorders.