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The Staphylococcus aureus biofilm extracellular matrix (ECM) is a complex, self-produced scaffold of extracellular polymeric substances (EPS) that encases bacterial communities (Otto, M., 2008). It is primarily composed of the polysaccharide intercellular adhesin (PIA/PNAG), extracellular DNA (eDNA), and various surface proteins and amyloid fibers, such as phenol-soluble modulins (Arciola, C. R., et al., 2018; Moormeier, D. E., & Bayles, K. W., 2017). This matrix serves as a physical and chemical barrier that protects the bacteria from host immune defenses and significantly increases tolerance to conventional antibiotics by limiting diffusion and creating metabolic microenvironments (Sultan, A. R., et al., 2022). In clinical settings, the S. aureus biofilm ECM is a major factor in the persistence of chronic infections, such as those involving medical implants, heart valves (endocarditis), and bone tissue (osteomyelitis). Therapeutic strategies targeting the ECM aim to degrade its structural components using enzymes like DNase I or glycoside hydrolases (e.g., Dispersin B), thereby disrupting the biofilm's integrity to allow antibiotics and immune cells to reach the embedded bacteria (Kaplan, J. B., 2010). This approach is often combined with standard antimicrobial therapy to improve clearance of recalcitrant infections.
Enzymatic degradation of matrix components (e.g., PNAG, eDNA, proteins) to disrupt structural integrity, promote bacterial dispersal, and enhance antibiotic penetration (Kaplan, J. B., 2010; Sultan, A. R., et al., 2022).
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