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Microbial biofilm matrix components, primarily referred to as the extracellular polymeric substance (EPS), form the structural and functional scaffold of microbial communities (Flemming & Wingender, 2010). This matrix is a complex assembly of exopolysaccharides, proteins, extracellular DNA (eDNA), and lipids that provides mechanical stability and mediates adhesion to various surfaces (Karygianni et al., 2020). Beyond its structural role, the EPS acts as a protective barrier, shielding embedded pathogens from the host immune system and significantly increasing resistance to antimicrobial agents (Hall & Mah, 2017). In clinical settings, the biofilm matrix is a hallmark of chronic and recalcitrant infections, including those associated with cystic fibrosis, chronic wounds, and medical implants (Donlan, 2001). Therapeutic strategies targeting these components involve the use of enzymes like DNases or glycoside hydrolases to degrade the matrix, or chelating agents to destabilize its architecture (Tetz et al., 2009). By disrupting the EPS, these treatments aim to disperse the biofilm, thereby enhancing the penetration of antibiotics and facilitating the clearance of the infection by the host (Boles & Horswill, 2008).
Degradation of extracellular DNA, enzymatic hydrolysis of exopolysaccharides, chelation of stabilizing metal ions, and inhibition of matrix synthesis to disrupt biofilm structural integrity and enhance antimicrobial penetration (Flemming & Wingender, 2010; Tetz et al., 2009).
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