Molecular response to the non-lytic peptide bac7 (1-35) triggers disruption of Klebsiella pneumoniae biofilm.

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, b

SUBMITTER: Beckman I V RL 

PROVIDER: S-EPMC12677791 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature