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<p><i>Pseudomonas aeruginosa</i> is an opportunistic pathogen that can cause severe infections in immunocompromised patients. N-(3-oxo-dodecanoyl) homoserine lactone (3oc12) is a small quorum molecule that is used to communicate between bacterial cells and between bacteria and the host. However, the exact molecular mechanisms of this exchange is not yet fully understood. Here, we present a modality that <i>P. aeruginosa</i> uses to finetune the severity of lung infection, where 3oc12 is incorporated into the host cell membrane, causing a marked increase in epidermal growth factor receptor (EGFR) ligand-independent self-dimerization. This ligand-free self-activation leads to epidermal growth factor receptor-signal transducer activator of transcription-3 (EGFR-STAT3) signaling, resulting in higher expression of tight junction proteins. This effect reduces the permeability of lung epithelial barrier, which in turn inhibits the release of <i>P. aeruginosa</i> from alveoli into the systemic circulation, and is essential to the establishment of long-term infection. This finding suggests a new, pathogen-autonomous mechanism to describe a tendency of <i>P. aeruginosa</i> of maintaining persistent chronic infection.</p>

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A Pseudomonas aeruginosa quorum-sensing inducer controls lung permeability in establishing chronic infection via EGFR

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月9日

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  • Mingke Zheng,
  • Jie Chen,
  • Gege Qin,
  • Ze Zhang,
  • Di Zhai,
  • Hefei Ruan,
  • Tie Xia,
  • Tongtao Yue,
  • Yan Shi

摘要

Pseudomonas aeruginosa is an opportunistic pathogen that can cause severe infections in immunocompromised patients. N-(3-oxo-dodecanoyl) homoserine lactone (3oc12) is a small quorum molecule that is used to communicate between bacterial cells and between bacteria and the host. However, the exact molecular mechanisms of this exchange is not yet fully understood. Here, we present a modality that P. aeruginosa uses to finetune the severity of lung infection, where 3oc12 is incorporated into the host cell membrane, causing a marked increase in epidermal growth factor receptor (EGFR) ligand-independent self-dimerization. This ligand-free self-activation leads to epidermal growth factor receptor-signal transducer activator of transcription-3 (EGFR-STAT3) signaling, resulting in higher expression of tight junction proteins. This effect reduces the permeability of lung epithelial barrier, which in turn inhibits the release of P. aeruginosa from alveoli into the systemic circulation, and is essential to the establishment of long-term infection. This finding suggests a new, pathogen-autonomous mechanism to describe a tendency of P. aeruginosa of maintaining persistent chronic infection.