AI Article Synopsis
- Hypervirulent bacteria produce more extracellular polysaccharides, which form resilient biofilms that can be disrupted by the peptide bactenecin 7 (bac7 (1-35)).
- Treatment with bac7 (1-35) causes the biofilm matrix to collapse, leading to the release and subsequent killing of bacterial cells.
- Research identifies specific regions of bac7 (1-35) that interact with polysaccharides, demonstrating its effectiveness in reducing bacterial levels in a murine skin abscess model.
Article Abstract
Hypervirulent is known for its increased extracellular polysaccharide production. Biofilm matrices of hypervirulent have increased polysaccharide abundance and are uniquely susceptible to disruption by peptide bactenecin 7 (bac7 (1-35)). Here, using confocal microscopy, we show that polysaccharides within the biofilm matrix collapse following bac7 (1-35) treatment. This collapse led to the release of cells from the biofilm, which were then killed by the peptide. Characterization of truncated peptide analogs revealed that their interactions with polysaccharide were responsible for the biofilm matrix changes that accompany bac7 (1-35) treatment. Ultraviolet photodissociation mass spectrometry with the parental peptide or a truncated analog bac7 (10-35) reveal the important regions for bac7 (1-35) complexing with polysaccharides. Finally, we tested bac7 (1-35) using a murine skin abscess model and observed a significant decrease in the bacterial burden. These findings unveil the potential of bac7 (1-35) polysaccharide interactions to collapse biofilms.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11008256 | PMC |
| http://dx.doi.org/10.1016/j.xcrp.2024.101869 | DOI Listing |
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