ArticleCurrent microbiology2026
Caerin 1.1/1.9 Inhibits Growth and Biofilm Formation of Carbapenem-Resistant Klebsiella pneumoniae and Induces Coordinated Transcriptomic Stress Responses.
Article in Current microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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12 authors.
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Abstract
Carbapenem-resistant Klebsiella pneumoniae (CRKP) is a major cause of healthcare-associated infections and a World Health Organization critical-priority pathogen due to extensive antimicrobial resistance and limited treatment options. Host-defense peptides represent promising alternatives to conventional antibiotics because of their broad-spectrum activity and low propensity for resistance development. Here, we evaluated the antibacterial activity of a fixed 1:1 combination of the frog-derived peptides caerin 1.1 and caerin 1.9 (F1/F3) against a reference K. pneumoniae strain and four clinical CRKP isolates. Individually, F1 and F3 exhibited MICs of 12 µM against the reference strain, whereas the F1/F3 combination reduced the MIC to 5 µM and showed an additive antibacterial interaction. F1/F3 retained activity against clinical CRKP isolates with strain-dependent susceptibility and inhibited biofilm formation and reduced pre-established biofilm biomass in a concentration-dependent manner. Scanning electron microscopy revealed pronounced morphological and surface alterations following peptide treatment. Transcriptomic analysis demonstrated broad bacterial responses to F1/F3 exposure, including downregulation of genes associated with ribosomal function, protein synthesis, metabolism, and oxidative phosphorylation, together with activation of stress-response pathways and differential expression of predicted small regulatory RNAs. SNP analysis revealed no evidence of increased mutation burden following peptide exposure. These findings demonstrate the antibacterial potential of F1/F3 against CRKP and provide insights into bacterial responses associated with caerin peptide treatment.
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