ArticlePLoS pathogens2025
Molecular response to the non-lytic peptide bac7 (1-35) triggers disruption of Klebsiella pneumoniae biofilm.
Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Liposome-Mediated Bacterial Ferroptosis-like Death: A Novel Paradigm for Antimicrobial Therapy.Antibiotics (Basel, Switzerland) · 2026Review
- Correction: Molecular response to the non-lytic peptide bac7 (1-35) triggers disruption of Klebsiella pneumoniae biofilm.PLoS pathogens · 2026Article
- Characterization of Proline-Rich Antimicrobial Peptides with SbmA Transporter-Dependent and Independent Antimicrobial Activity towardACS infectious diseases · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
13 authors.
Funding
Abstract
Klebsiella pneumoniae is becoming increasingly difficult to treat as multidrug-resistant (MDR) strains become more prevalent. The formation of biofilm heightens this threat by embedding bacterial cells in a polysaccharide-rich matrix that limits antibiotic penetration. Here we dissect the anti-biofilm bovine host-defense cathelicidin peptide fragment bac7 (1-35), exploring its anti-biofilm mechanism, evaluating its ability to curb colonization of the vital organs by hypervirulent K. pneumoniae, and testing its breadth of activity against diverse clinical isolates. Transcriptomic profiling revealed that bac7 (1-35) simultaneously compromises the bacterial membrane and inhibits ribosomal function, a dual assault that precipitates rapid biofilm collapse and blocks bacterial spread. Further, bac7 (1-35) eradicated the strongest biofilms produced by MDR clinical isolates in the Multidrug-Resistant Organism Repository and Surveillance Network (MRSN) diversity panel. Although bac7 (1-35) kills bacterial cells via a cytosolic mechanism, membrane interaction profiles varied among MRSN isolates, correlating with differential peptide translocation. In a delayed-treatment murine skin-abscess model, bac7 (1-35) halted in vivo colonization of the vital organs by the hypervirulent strain NTUH-K2044. Collectively, these results delineate a multifaceted mode of action for bac7 (1-35) and underscore its therapeutic promise against biofilm-associated MDR K. pneumoniae infections.
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Registered trials
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