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<p>The rapid emergence of multidrug-resistant (MDR) bacteria poses a critical challenge in hospital-acquired infections, particularly methicillin-resistant <i>Staphylococcus aureus</i> (MRSA) pneumonia. Antimicrobial peptides (AMPs) are promising therapeutic candidates due to their broad-spectrum antibacterial activity. Here, we report AMP-36, a 36-amino acid antimicrobial peptide rationally designed and synthesized from SAAP-148, exhibits potent antibacterial activity. AMP-36 displayed low micromolar minimum inhibitory concentrations and rapid bactericidal activity in vitro, achieving near-complete bacterial killing within 8&#xa0;h. In the murine pneumonia model, AMP-36 significantly reduced bacterial burden in bronchoalveolar lavage fluid (BALF) and markedly alleviated lung inflammation. Scanning electron microscopy (SEM) revealed pronounced disruption of MRSA cell membranes following AMP-36 treatment, indicating membrane damage as the primary antibacterial mechanism. Transcriptomic analysis further demonstrated its broad transcriptional alterations. Collectively, these findings highlight AMP-36 as a promising therapeutic candidate for MRSA pneumonia and provide mechanistic insights into its antimicrobial action.</p>

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AMP-36 exhibits potent therapeutic efficacy against MRSA pneumonia through membrane-target mechanism

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月17日

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  • Yanxiao Han,
  • Yuli Wang,
  • Lin Cheng,
  • Chenxi Sun,
  • Jialin Song,
  • Xunqi Zhang,
  • Xuhua Zhang,
  • Yang Jiang,
  • Xiaoyan Li,
  • Dexiao Kong,
  • Chengyun Zheng

摘要

The rapid emergence of multidrug-resistant (MDR) bacteria poses a critical challenge in hospital-acquired infections, particularly methicillin-resistant Staphylococcus aureus (MRSA) pneumonia. Antimicrobial peptides (AMPs) are promising therapeutic candidates due to their broad-spectrum antibacterial activity. Here, we report AMP-36, a 36-amino acid antimicrobial peptide rationally designed and synthesized from SAAP-148, exhibits potent antibacterial activity. AMP-36 displayed low micromolar minimum inhibitory concentrations and rapid bactericidal activity in vitro, achieving near-complete bacterial killing within 8 h. In the murine pneumonia model, AMP-36 significantly reduced bacterial burden in bronchoalveolar lavage fluid (BALF) and markedly alleviated lung inflammation. Scanning electron microscopy (SEM) revealed pronounced disruption of MRSA cell membranes following AMP-36 treatment, indicating membrane damage as the primary antibacterial mechanism. Transcriptomic analysis further demonstrated its broad transcriptional alterations. Collectively, these findings highlight AMP-36 as a promising therapeutic candidate for MRSA pneumonia and provide mechanistic insights into its antimicrobial action.