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

AMP-36 通过膜靶向机制对耐甲氧西林金黄色葡萄球菌肺炎表现出强大的治疗功效。

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Abstract

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. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-44156-6.

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