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<p>The global burden of pulmonary fibrosis is increasing. Recent studies have shown that some pulmonary fibrotic lesions caused by COVID-19 infection may persist for a long time. Emerging evidence suggested a critical association between gut microbiota and pulmonary fibrosis. In this study, the clinical follow-up data from post-COVID-19 patients indicated that those with higher CT image scores were older, had a significantly lower <i>Blautia</i> and <i>Bifidobacterium</i> to <i>Streptococcus</i> ratio (B/S index). We examined whether <i>Bifidobacterium adolescentis</i> could attenuate bleomycin-induced pulmonary fibrosis in mice, with particular attention in the aging mice. Aging mice exhibited more severe pulmonary fibrosis after BLM induction, while the intervention of <i>B. adolescentis</i> attenuated the degree of pulmonary fibrosis in aging mice to a state similar to that of young mice. <i>B. adolescentis</i> alleviated inflammatory responses by enhancing the gut barrier, and reduced fibrotic marker expression (TGF-β, IL-17, α-SMA, Collagen I/III) by modulating PPAR and Th17 signaling pathways. Furthermore, <i>B. adolescentis</i> stabilized gut microbiota and increased the abundance of <i>Bifidobacterium</i>, <i>Turicibacter</i>, and <i>norank_f_Desulfovibrionaceae</i>, thereby suppressed the prostaglandin E2 (PGE2) and affected collagen deposition. <i>B. adolescentis</i> alleviates pulmonary fibrosis through the gut-lung axis by regulating PGE2/PPAR/Th17 signaling, providing a promising therapeutic approach for pulmonary fibrosis management.</p>

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B. adolescentis alleviates inflammation and suppresses PGE2 through remodling gut microbiota to attenuate pulmonary fibrosis in aging mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月24日

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  • Jiali Ni,
  • Fengjiao Wang,
  • Yechen Wu,
  • Jian Shen,
  • Ziyuan Zhou,
  • Lvwan Xu,
  • Zhuoqi Lou,
  • Yangfan Shen,
  • Bo Qiu,
  • Qiangqiang Xiang,
  • Pengyu Yin,
  • Yanfei Chen,
  • Lanjuan Li

摘要

The global burden of pulmonary fibrosis is increasing. Recent studies have shown that some pulmonary fibrotic lesions caused by COVID-19 infection may persist for a long time. Emerging evidence suggested a critical association between gut microbiota and pulmonary fibrosis. In this study, the clinical follow-up data from post-COVID-19 patients indicated that those with higher CT image scores were older, had a significantly lower Blautia and Bifidobacterium to Streptococcus ratio (B/S index). We examined whether Bifidobacterium adolescentis could attenuate bleomycin-induced pulmonary fibrosis in mice, with particular attention in the aging mice. Aging mice exhibited more severe pulmonary fibrosis after BLM induction, while the intervention of B. adolescentis attenuated the degree of pulmonary fibrosis in aging mice to a state similar to that of young mice. B. adolescentis alleviated inflammatory responses by enhancing the gut barrier, and reduced fibrotic marker expression (TGF-β, IL-17, α-SMA, Collagen I/III) by modulating PPAR and Th17 signaling pathways. Furthermore, B. adolescentis stabilized gut microbiota and increased the abundance of Bifidobacterium, Turicibacter, and norank_f_Desulfovibrionaceae, thereby suppressed the prostaglandin E2 (PGE2) and affected collagen deposition. B. adolescentis alleviates pulmonary fibrosis through the gut-lung axis by regulating PGE2/PPAR/Th17 signaling, providing a promising therapeutic approach for pulmonary fibrosis management.