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Bacterial and fungal biofilm matrices are complex, self-produced extracellular structures composed of polysaccharides, proteins, and extracellular DNA (eDNA) that house and protect microbial communities (Flemming & Wingender, 2010). These matrices act as a physical and chemical barrier, significantly increasing the tolerance of embedded microorganisms to both the host immune system and conventional antimicrobial therapies by up to 1000-fold (Donlan, 2002). Biofilms are a hallmark of chronic and recalcitrant infections, frequently colonizing medical devices, chronic wounds, and mucosal surfaces in diseases like cystic fibrosis (Koo et al., 2017). Therapeutic interventions targeting the biofilm matrix focus on enzymatic degradation of EPS components, inhibition of quorum sensing pathways, or the use of chelating agents to destabilize the structural integrity of the matrix (Koo et al., 2017). By breaking down this protective shield, these biofilm-disrupting agents aim to restore the efficacy of antibiotics and facilitate the eradication of the underlying infection by host defenses.
Degradation of extracellular polymeric substances (EPS) such as eDNA and polysaccharides, inhibition of quorum sensing signaling pathways, and disruption of microbial cell-to-cell or cell-to-surface adhesion to enhance antimicrobial penetration and host immune clearance.
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