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                <identifier>oai:data.mendeley.com/2v95m3ycr6.1</identifier>
                <datestamp>2026-09-15T09:21:46Z</datestamp>
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    <dc:creator>XIE, Xiaobao</dc:creator>
    <dc:title>H₂S-Driven Copper Redox Cycling Integrates Direct Bactericidal Activity and Macrophage Immunomodulation for Enhanced MRSA Clearance at Low-dose Copper</dc:title>
    <dc:publisher>Mendeley Data</dc:publisher>
    <dc:description>This study reports a hydrogen sulfide (H₂S)-driven copper redox cycling system that synergizes direct bactericidal activity and macrophage immunomodulation for methicillin-resistant Staphylococcus aureus (MRSA) clearance in vitro at subtoxic copper doses. By coupling oxygen-mediated oxidation with sulfide-driven reduction, the system achieves self-sustaining Cu(II)/Cu(I) cycling, maintaining bioactive Cu(I) regeneration (30.8–50.6% reduction efficiency over 8 d) under physiological redox equilibrium. At an ultralow total copper dose (12.5 μM), the dual-action mechanism delivered 67.3% inhibition of extracellular MRSA growth in vitro, alongside 86.1% clearance of intracellular MRSA in cultured RAW264.7 macrophages, concomitant with Cu(I)-associated M1 polarization. Comparative in vitro assays demonstrated markedly enhanced intracellular MRSA clearance relative to Cu(II) monotherapy (86.1% vs. 14.3%), alongside M1 activation characterized by TNF-α upregulation (ELISA), IL-10 suppression in M2-polarized cells, and an M2-to-M1 phenotype transition (qRT-PCR). The system preserved host cell viability (&gt;80%) in vitro and was associated with reduced MRSA-induced M2 polarization. These in vitro findings propose a metal-based antimicrobial strategy that integrates pathogen-targeting and host-directed actions and supports further evaluation of copper-dose reduction; efficacy in an infection model remains to be established.</dc:description>
    <dc:subject>Microbiology</dc:subject>
    <dc:subject>Biochemistry Application</dc:subject>
    <dc:subject>Copper</dc:subject>
    <dc:subject>Antimicrobial Resistance</dc:subject>
    <dc:subject>Macrophage Polarization</dc:subject>
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    <dc:identifier>doi:10.17632/2v95m3ycr6.1</dc:identifier>
    <dc:identifier>oai:data.mendeley.com/2v95m3ycr6.1</dc:identifier>
    <dc:rights>Creative Commons Attribution 4.0 International</dc:rights>
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    <dc:date>2026-09-15T09:21:46Z</dc:date>
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