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Microbial biofilms are complex, multicellular communities of microorganisms embedded within a self-produced extracellular polymeric substance (EPS) matrix. This matrix is primarily composed of polysaccharides, proteins, and extracellular DNA (eDNA), which provide structural stability and act as a protective barrier against host immune defenses and antimicrobial agents (Flemming & Wingender, 2010). Biofilms are central to the pathogenesis of chronic infections, such as those found in cystic fibrosis, chronic wounds, and on indwelling medical devices like catheters and prosthetic joints (Costerton et al., 1999). Therapeutic strategies targeting the biofilm matrix aim to degrade its structural components or inhibit its formation, thereby transitioning the microbes from a protected sessile state to a more vulnerable planktonic state. For example, enzymes like Dornase alfa (DNase I) target eDNA to reduce matrix viscosity, while chelating agents like EDTA disrupt the ionic cross-linking of polysaccharides (Donlan, 2002). By compromising the physical integrity of the biofilm, these treatments enhance the efficacy of co-administered antibiotics and facilitate clearance by the host immune system.
Enzymatic degradation of extracellular polymeric substances (e.g., eDNA, polysaccharides), chelation of divalent cations to destabilize matrix integrity, and inhibition of quorum sensing to prevent biofilm maturation.
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