ClpB regulates biofilm formation and improves wound healing in MRSA, suggesting its potential as an anti-biofilm target.
Introduction This study aims to explore the effects of the molecular chaperone ClpB on the biofilm formation and pathogenicity of methicillin-resistant Staphylococcus aureus (MRSA). Methods The biological membrane formation was evaluated by constructing a clpB knockout strain (Δ clpB ) and a complemented strain (CΔ clpB ) of USA300 MRSA, followed by crystal violet staining, scanning electron microscopy, confocal laser scanning microscopy, and quantitative analysis of extracellular matrix components. A mouse skin infection model was subsequently employed to assess wound healing, histopathological changes, and the expression levels of inflammatory factors. Results The results showed that compared with the wild strain (WT), the biomass of Δ clpB biofilm was significantly reduced ( p < 0.0001), the structure was damaged and the production of extracellular matrix (eDNA, polysaccharides, proteins) decreased. CΔ clpB then returned to the WT level. In the in vivo experiments, the Δ clpB infection group had faster wound healing, reduced tissue damage, and decreased expressions of TNF- α and IL-6 at both protein and mRNA levels. Conclusion ClpB promotes the formation of MRSA biofilms by regulating extracellular matrix synthesis and host inflammatory responses and is a potential target for anti-biofilm therapy.
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