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<p><i>Mycoplasma pneumoniae</i> (Mp) is a major pathogen of community-acquired pneumonia increasingly resistant to macrolides. Mp infection provokes oxidative stress, disrupts epithelial integrity, and skews T helper (Th) cell balance through CARDS toxin–mediated immune dysregulation. Here, we investigated the protective effects of melatonin, a pleiotropic hormone with antioxidant and immunomodulatory functions, in patients and a murine model of Mp pneumonia. Mp infection perturbed the local Th1/Th2/Th17 balance, accompanied by ROS accumulation, CXCL10-induced TLR4/STAT1 activation, and loss of ZO1-dependent tight junctions. Melatonin administration suppressed ROS production, restored epithelial barrier integrity, and rebalanced Th responses within the airway microenvironment. Mechanistically, melatonin inhibited CXCL10–TLR4/STAT1 signaling, with TLR4 residue A366 identified as a key regulatory site. These findings reveal that melatonin alleviates Mp-induced airway injury by maintaining immune and epithelial homeostasis, highlighting its potential as an adjunctive therapy for macrolide-resistant Mp pneumonia.</p>

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Melatonin attenuates Mycoplasma pneumoniae-Induced Inflammation and barrier dysfunction by CXCL10/TLR4/STAT1 axis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月23日

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  • Chun-Yi Lee,
  • Tsung-Hua Wu,
  • Meei-Ling Sheu,
  • Wen-Hsuan Chiang,
  • Hung-Chuan Pan,
  • Yu-Ping Fang,
  • Yi-Ching Tsai,
  • Chia-Yun Tsai,
  • De-Wei Lai

摘要

Mycoplasma pneumoniae (Mp) is a major pathogen of community-acquired pneumonia increasingly resistant to macrolides. Mp infection provokes oxidative stress, disrupts epithelial integrity, and skews T helper (Th) cell balance through CARDS toxin–mediated immune dysregulation. Here, we investigated the protective effects of melatonin, a pleiotropic hormone with antioxidant and immunomodulatory functions, in patients and a murine model of Mp pneumonia. Mp infection perturbed the local Th1/Th2/Th17 balance, accompanied by ROS accumulation, CXCL10-induced TLR4/STAT1 activation, and loss of ZO1-dependent tight junctions. Melatonin administration suppressed ROS production, restored epithelial barrier integrity, and rebalanced Th responses within the airway microenvironment. Mechanistically, melatonin inhibited CXCL10–TLR4/STAT1 signaling, with TLR4 residue A366 identified as a key regulatory site. These findings reveal that melatonin alleviates Mp-induced airway injury by maintaining immune and epithelial homeostasis, highlighting its potential as an adjunctive therapy for macrolide-resistant Mp pneumonia.