Antimicrobial peptide-induced inner membrane hyperpolarization is associated with antibiotic sensitization and attenuated MIC escalation in multidrug-resistant Gram-negative pathogens

抗菌肽诱导的内膜超极化与多重耐药革兰氏阴性病原体的抗生素敏感性增强和MIC值上升减弱有关。

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Abstract

Antimicrobial resistance and dysregulated inflammation drive mortality in multidrug-resistant (MDR) sepsis. We evaluated the cationic peptide TP2-5 as a low-dose antibiotic adjuvant. At sub-MIC concentrations, TP2-5 enhanced antibiotic susceptibility of MDR E. coli in broth and 50% human serum, and in combination with antibiotics was associated with attenuated MIC escalation during 21-day serial passage. Membrane potential assays and cryo-electron tomography showed envelope perturbation characterized by inner-membrane hyperpolarization. This biophysical state was temporally associated with preferential interactions with lipopolysaccharide (LPS) and anionic phospholipids rather than nonspecific permeabilization. TP2-5 neutralized LPS and reduced TLR4-dependent cytokine production. In our murine polymicrobial CLP sepsis model, TP2-5 alone or with meropenem achieved 100% survival, accompanied by reduced bacterial burden and systemic inflammatory cytokines, consistent with combined antibacterial and host-directed effects, supporting a multifunctional adjuvant profile. This study did not measure bacterial membrane potential in vivo, and the causal role of hyperpolarization in protection or attenuated MIC escalation remains to be determined.

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