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<p>Pneumonia, characterized by infection-induced inflammation of the lungs, poses a significant health burden, particularly among children. ADP ribosylation factor 3 (ARF3) is a key regulatory protein implicated in various pathological processes; however, its role in pneumonia caused by influenza A virus (IAV) remains inadequately understood. In this study, we demonstrated that ARF3 expression was upregulated in a young mouse model of IAV-induced pneumonia. Knockdown of ARF3 effectively mitigated lung injury in this model. Furthermore, suppression of ARF3 expression alleviated pulmonary inflammation by reducing the levels of pro-inflammatory cytokines, including TNF-α, IL-6, and IL-1β. In vitro experiments further revealed that ARF3 downregulation inhibited replication of the H3N2 IAV strain. Notably, ARF3 knockdown also attenuated NLRP3 inflammasome activation, a key mediator of inflammatory responses. Collectively, these findings provide the first evidence that ARF3 knockdown suppresses both IAV replication and virus-induced pneumonia by modulating inflammasome activation, suggesting that ARF3 may serve as a potential therapeutic target for pneumonia intervention.</p> Graphical abstract <p></p>

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ARF3 knockdown inhibits influenza a virus and virus-induced pneumonia

  • 期刊论文

  • 发表日期：

    2025年7月3日

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  • Zhinan Zhang,
  • Banghao Lu,
  • Bihe Zeng

摘要

Pneumonia, characterized by infection-induced inflammation of the lungs, poses a significant health burden, particularly among children. ADP ribosylation factor 3 (ARF3) is a key regulatory protein implicated in various pathological processes; however, its role in pneumonia caused by influenza A virus (IAV) remains inadequately understood. In this study, we demonstrated that ARF3 expression was upregulated in a young mouse model of IAV-induced pneumonia. Knockdown of ARF3 effectively mitigated lung injury in this model. Furthermore, suppression of ARF3 expression alleviated pulmonary inflammation by reducing the levels of pro-inflammatory cytokines, including TNF-α, IL-6, and IL-1β. In vitro experiments further revealed that ARF3 downregulation inhibited replication of the H3N2 IAV strain. Notably, ARF3 knockdown also attenuated NLRP3 inflammasome activation, a key mediator of inflammatory responses. Collectively, these findings provide the first evidence that ARF3 knockdown suppresses both IAV replication and virus-induced pneumonia by modulating inflammasome activation, suggesting that ARF3 may serve as a potential therapeutic target for pneumonia intervention.

Graphical abstract