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The biofilm extracellular polymeric substance (EPS) matrix is a complex, self-produced scaffold composed of polysaccharides, proteins, extracellular DNA (eDNA), and lipids that encases microbial communities (Flemming & Wingender, 2010). It serves as the primary structural component of biofilms, providing mechanical stability and acting as a protective barrier against environmental stressors, host immune responses, and antimicrobial agents (Costerton et al., 1999). In clinical settings, the EPS matrix is a major contributor to the persistence of chronic infections, such as those found in cystic fibrosis lungs or on indwelling medical devices, by significantly reducing the penetration and efficacy of conventional antibiotics (Koo et al., 2017). Therapeutic strategies targeting the biofilm matrix focus on degrading its structural components—for instance, using DNases to target eDNA or glycoside hydrolases to break down polysaccharides—thereby weakening the biofilm and sensitizing the resident bacteria to treatment (Tetz et al., 2009; Whitchurch et al., 2002). Understanding the interfaces between the matrix and the underlying surfaces is also critical for preventing initial bacterial attachment and subsequent biofilm maturation (Flemming & Wingender, 2010).
Enzymatic degradation of extracellular DNA and polysaccharides, chelation of divalent cations to destabilize the matrix, and physical disruption of the biofilm architecture to facilitate antimicrobial penetration (Tetz et al., 2009; Koo et al., 2017).
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