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<p>Interferon regulatory factor 5 (IRF5) is a key regulator of inflammatory responses; however, its role in chronic obstructive pulmonary disease remains unknown. A previous study showed increased IRF5 expression in the lungs of cigarette smoke (CS)-induced emphysema. Here we investigated the function of IRF5 in emphysema using <i>Irf5-</i>knockout (KO) mice. Alveolar destruction, inflammatory cell infiltration, cytokine levels and pyroptosis-related gene expression were assessed in CS-induced emphysema. To investigate the role of immune cells, Ly6C<sup>++</sup> (Ly6C<sup>high</sup>) monocytes and Ly6C<sup>high</sup> T cells from <i>Irf5-</i>KO mice were introduced into emphysema mice. The correlation between IRF5 levels and emphysema in humans was also evaluated. <i>Irf5</i>-KO mice showed decreased alveolar destruction after CS exposure. NLRP3 expression was suppressed, and gasdermin D cleavage was altered in <i>Irf5-</i>KO mice, suggesting a protective effect against pyroptotic cell death. Moreover, Ly6C<sup>high</sup> monocytes and Ly6C<sup>high</sup> T cells were more abundant in the lungs of <i>Irf5-</i>KO mice after CS exposure, and their transfer attenuated NLRP3 expression and alveolar damage. Furthermore, IRF5 expression was significantly elevated in lung tissues from patients. Our findings highlight IRF5 as a critical regulator of emphysema pathogenesis via NLRP3-mediated pyroptosis and Ly6C<sup>high</sup>-expressing immune cells. Targeting IRF5 may be a potential therapeutic strategy for chronic obstructive pulmonary disease.</p>

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Interferon regulatory factor 5 involves the pathogenesis of emphysema through NLRP3 and Ly6C expressing cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月5日

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  • Sun-Hee Heo,
  • Suk Young Park,
  • Na Hyun Kim,
  • Heeseo Kim,
  • In-Jeoung Baek,
  • Young Hoon Sung,
  • Chiwook Chung,
  • Sei Won Lee

摘要

Interferon regulatory factor 5 (IRF5) is a key regulator of inflammatory responses; however, its role in chronic obstructive pulmonary disease remains unknown. A previous study showed increased IRF5 expression in the lungs of cigarette smoke (CS)-induced emphysema. Here we investigated the function of IRF5 in emphysema using Irf5-knockout (KO) mice. Alveolar destruction, inflammatory cell infiltration, cytokine levels and pyroptosis-related gene expression were assessed in CS-induced emphysema. To investigate the role of immune cells, Ly6C++ (Ly6Chigh) monocytes and Ly6Chigh T cells from Irf5-KO mice were introduced into emphysema mice. The correlation between IRF5 levels and emphysema in humans was also evaluated. Irf5-KO mice showed decreased alveolar destruction after CS exposure. NLRP3 expression was suppressed, and gasdermin D cleavage was altered in Irf5-KO mice, suggesting a protective effect against pyroptotic cell death. Moreover, Ly6Chigh monocytes and Ly6Chigh T cells were more abundant in the lungs of Irf5-KO mice after CS exposure, and their transfer attenuated NLRP3 expression and alveolar damage. Furthermore, IRF5 expression was significantly elevated in lung tissues from patients. Our findings highlight IRF5 as a critical regulator of emphysema pathogenesis via NLRP3-mediated pyroptosis and Ly6Chigh-expressing immune cells. Targeting IRF5 may be a potential therapeutic strategy for chronic obstructive pulmonary disease.