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<p>Mitochondria are required for protecting host against pathogenic bacteria by activating mitochondrial unfolded protein response (UPR<sup>mt</sup>). Chlorogenic acid (CGA), a phenolic acid compound of green coffee extracts and tea has been shown to exhibit activities such as antioxidant, antibacterial, hepatoprotective, cardioprotective, anti-inflammatory, neuroprotective, anti-obesity. However, whether CGA regulates innate immunity and the underlying molecular mechanisms remain unknown. In this study, we found that CGA increased resistance to Gram-negative pathogen <i>Pseudomonas aeruginosa</i> PA14 in dose dependent manner. Meanwhile, CGA enhanced innate immunity in <i>Caenorhabditis elegans</i> by reducing intestinal bacterial burden. CGA also inhibited the proliferation of pathogenic bacteria. Importantly, CGA inhibited the production of <i>Pseudomonas</i> toxin pyocyanin (PYO) to protect <i>C. elegans</i> from <i>P. aeruginosa</i> PA14 infection. Furthermore, CGA activated the UPR<sup>mt</sup> and expression of antibacterial peptide genes to promote innate immunity in <i>C. elegans</i> via transcription factor ATFS-1(activating transcription factor associated with stress-1). Unexpectedly, CGA enhanced innate immunity independently of other known innate immune pathways. Intriguingly, CGA also protected mice from <i>P. aeruginosa</i> PA14 infection and activated UPR<sup>mt</sup>. Our work revealed a conserved mechanism by which CGA promoted innate immunity and boosted its therapeutic application in the treatment of pathogen infection.</p>

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Chlorogenic acid inhibits Pseudomonas toxin pyocyanin and activates mitochondrial UPR to protect host against pathogen infection

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年2月14日

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  • Yi Xiao,
  • Linlu Li,
  • Chao Han,
  • Tingyun Huang,
  • Shuangjie Ren,
  • Xiaoqin Wang,
  • Qianlu Xing,
  • Fang Liu

摘要

Mitochondria are required for protecting host against pathogenic bacteria by activating mitochondrial unfolded protein response (UPRmt). Chlorogenic acid (CGA), a phenolic acid compound of green coffee extracts and tea has been shown to exhibit activities such as antioxidant, antibacterial, hepatoprotective, cardioprotective, anti-inflammatory, neuroprotective, anti-obesity. However, whether CGA regulates innate immunity and the underlying molecular mechanisms remain unknown. In this study, we found that CGA increased resistance to Gram-negative pathogen Pseudomonas aeruginosa PA14 in dose dependent manner. Meanwhile, CGA enhanced innate immunity in Caenorhabditis elegans by reducing intestinal bacterial burden. CGA also inhibited the proliferation of pathogenic bacteria. Importantly, CGA inhibited the production of Pseudomonas toxin pyocyanin (PYO) to protect C. elegans from P. aeruginosa PA14 infection. Furthermore, CGA activated the UPRmt and expression of antibacterial peptide genes to promote innate immunity in C. elegans via transcription factor ATFS-1(activating transcription factor associated with stress-1). Unexpectedly, CGA enhanced innate immunity independently of other known innate immune pathways. Intriguingly, CGA also protected mice from P. aeruginosa PA14 infection and activated UPRmt. Our work revealed a conserved mechanism by which CGA promoted innate immunity and boosted its therapeutic application in the treatment of pathogen infection.