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<p>Patients with a history of <i>Mycobacterium tuberculosis</i> infection often suffer from irreversible and progressive pulmonary damage, yet the underlying mechanisms are not fully understood. Here we conducted single-cell transcriptomic analysis of human lung tissues including 19 post-tuberculosis lung tissues and 13 matched normal lung samples as controls, focusing on areas within and surrounding tuberculosis lesions. We identified tuberculosis-associated molecular signatures across various cell types, including gene expression patterns associated with senescence, inflammation, fibrosis and apoptosis. We observed increased vascular inflammation as a key feature of lung tissues following tuberculosis. Signatures of decreased FOXO3 signalling and increased NF-κB-dependent thromboinflammation were validated by showing that small interfering RNA silencing of FOXO3 and thrombin treatment exacerbated senescence and inflammation in pulmonary endothelial cells. These findings provide insight into the mechanisms contributing to post-tuberculosis pulmonary damage and suggest potential therapeutic targets for alleviating lung impairment in these patients.</p>

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A single-cell transcriptomic atlas reveals senescence and inflammation in the post-tuberculosis human lung

  • 期刊论文

  • 发表日期：

    2025年7月14日

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  • Guoqiang Sun,
  • Kuan Li,
  • Jiale Ping,
  • Liyun Zhao,
  • Chao Cui,
  • Junping Wu,
  • Lixin Xie,
  • Xiaojun Yao,
  • Gang Xu,
  • Shuai Ma,
  • Yanling Fan,
  • Qiaoran Wang,
  • Danlu Yang,
  • Bilan Luo,
  • Huiying Liu,
  • Jiayin Yang,
  • Weiqi Zhang,
  • Weihong Song,
  • Guoguang Zhao,
  • Xiaobing Fu,
  • Xiu-Wu Bian,
  • Jing Qu,
  • Si Wang,
  • Huaiyong Chen,
  • Guang-Hui Liu

摘要

Patients with a history of Mycobacterium tuberculosis infection often suffer from irreversible and progressive pulmonary damage, yet the underlying mechanisms are not fully understood. Here we conducted single-cell transcriptomic analysis of human lung tissues including 19 post-tuberculosis lung tissues and 13 matched normal lung samples as controls, focusing on areas within and surrounding tuberculosis lesions. We identified tuberculosis-associated molecular signatures across various cell types, including gene expression patterns associated with senescence, inflammation, fibrosis and apoptosis. We observed increased vascular inflammation as a key feature of lung tissues following tuberculosis. Signatures of decreased FOXO3 signalling and increased NF-κB-dependent thromboinflammation were validated by showing that small interfering RNA silencing of FOXO3 and thrombin treatment exacerbated senescence and inflammation in pulmonary endothelial cells. These findings provide insight into the mechanisms contributing to post-tuberculosis pulmonary damage and suggest potential therapeutic targets for alleviating lung impairment in these patients.