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The bacterial biofilm extracellular polymeric matrix (EPS) is a complex, self-produced three-dimensional scaffold composed of polysaccharides, proteins, lipids, and extracellular DNA (eDNA) that encases bacterial communities (Flemming & Wingender, 2010, Nature Reviews Microbiology). This matrix serves as the primary structural component of biofilms, providing mechanical stability and mediating adhesion to both biotic and abiotic surfaces, such as human tissues and medical implants. Biologically, the EPS acts as a protective barrier against environmental stressors, host immune responses, and antimicrobial agents, often rendering bacteria up to 1,000 times more resistant to antibiotics than their planktonic counterparts (Yan & Bassler, 2019, Cell Host & Microbe). It also facilitates cell-to-cell communication and nutrient sequestration, creating a stable microenvironment for bacterial persistence. In clinical settings, the EPS is a major factor in the pathogenesis of chronic infections, such as those found in cystic fibrosis lungs and chronic wounds (Ciofu et al., 2022, Nature Reviews Disease Primers). Therapeutic strategies targeting the EPS aim to degrade its structural components or inhibit its synthesis, thereby 'priming' the biofilm for clearance by conventional antibiotics or the host immune system. Examples of such interventions include the use of DNases to cleave eDNA or glycoside hydrolases to break down exopolysaccharides (Tetz et al., 2009, Antimicrobial Agents and Chemotherapy).
Enzymatic degradation of structural components such as extracellular DNA and polysaccharides, chelation of divalent cations (Ca2+, Mg2+) that stabilize the matrix, and inhibition of matrix synthesis to increase antibiotic penetration and immune cell access.
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