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<p>Asthma is a chronic inflammatory disease characterized by airway hyperresponsiveness, airway remodeling, and persistent inflammation, with neutrophilic phenotypes often associated with severe and steroid-resistant cases. SerpinB1, a serine protease inhibitor, has been shown to modulate inflammatory processes through its interaction with neutrophil elastase (Elane); however, its specific role in asthma pathogenesis has not been fully clarified. In the present study, we investigated the function of SerpinB1 in an ovalbumin (OVA)-induced mouse model of asthma as well as in lipopolysaccharide (LPS)-stimulated BEAS-2B cells. Expression analysis revealed that SerpinB1 was downregulated in asthmatic mice. Overexpression of SerpinB1 markedly alleviated neutrophil-driven airway inflammation, reduced structural remodeling of the airways, and suppressed pyroptosis, as demonstrated by decreased expression of caspase-1, GSDMD, IL-1β, and NLRP3. Co-immunoprecipitation and immunofluorescence assays further confirmed that SerpinB1 directly interacts with Elane. Importantly, knockdown of Elane abolished the protective effects conferred by SerpinB1, indicating that the regulation of asthma-related pathology by SerpinB1 is mediated through Elane inhibition. In conclusion, SerpinB1 may mitigate airway inflammation and remodeling in asthma by targeting Elane and suppressing pyroptosis, supporting it as a potential therapeutic target for neutrophil-dominant asthma.</p>

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SerpinB1 reduces neutrophil airway inflammation, airway remodeling, and pyroptosis in asthmatic mice by interacting with Elane

  • 期刊论文

  • 发表日期：

    2025年10月31日

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  • Na Chen,
  • Zhu Chen,
  • LianKe Li,
  • Zhiwei Liu,
  • Qiong Tao,
  • Weizhou Wang,
  • Yang Yang

摘要

Asthma is a chronic inflammatory disease characterized by airway hyperresponsiveness, airway remodeling, and persistent inflammation, with neutrophilic phenotypes often associated with severe and steroid-resistant cases. SerpinB1, a serine protease inhibitor, has been shown to modulate inflammatory processes through its interaction with neutrophil elastase (Elane); however, its specific role in asthma pathogenesis has not been fully clarified. In the present study, we investigated the function of SerpinB1 in an ovalbumin (OVA)-induced mouse model of asthma as well as in lipopolysaccharide (LPS)-stimulated BEAS-2B cells. Expression analysis revealed that SerpinB1 was downregulated in asthmatic mice. Overexpression of SerpinB1 markedly alleviated neutrophil-driven airway inflammation, reduced structural remodeling of the airways, and suppressed pyroptosis, as demonstrated by decreased expression of caspase-1, GSDMD, IL-1β, and NLRP3. Co-immunoprecipitation and immunofluorescence assays further confirmed that SerpinB1 directly interacts with Elane. Importantly, knockdown of Elane abolished the protective effects conferred by SerpinB1, indicating that the regulation of asthma-related pathology by SerpinB1 is mediated through Elane inhibition. In conclusion, SerpinB1 may mitigate airway inflammation and remodeling in asthma by targeting Elane and suppressing pyroptosis, supporting it as a potential therapeutic target for neutrophil-dominant asthma.