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The biofilm extracellular polymeric substance (EPS) matrix is a complex, self-produced scaffold composed of polysaccharides, proteins, lipids, and extracellular DNA (eDNA) that encases microbial communities (Flemming & Wingender, 2010). It serves as a critical physical and chemical barrier, protecting embedded pathogens from host immune cells and increasing antibiotic tolerance by up to 1,000-fold compared to planktonic cells (Ciofu et al., 2022). In clinical contexts, the EPS matrix is central to the persistence of chronic infections, such as those found in cystic fibrosis lungs, chronic wounds, and on medical devices like catheters and prosthetic joints (Karygianni et al., 2020). Therapeutic interventions targeting the matrix, such as the use of Dornase alfa to degrade eDNA or glycoside hydrolases to break down polysaccharides, aim to destabilize the biofilm structure (Tetz & Tetz, 2010). This disruption facilitates the penetration of conventional antibiotics and enhances the ability of the host's immune system to clear the infection.
The mechanism involves the enzymatic or chemical degradation of the structural components of the extracellular polymeric substance (EPS) matrix, such as extracellular DNA (eDNA) and polysaccharides, or the chelation of divalent cations (e.g., Ca2+, Mg2+) that stabilize the matrix (Flemming & Wingender, 2010). This disruption reduces the physical integrity and viscosity of the biofilm, increasing the diffusion of antibiotics to the embedded bacteria and exposing them to host immune clearance (Ciofu et al., 2022).
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