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The bacterial biofilm matrix is a complex, self-produced scaffold composed of extracellular polymeric substances (EPS), including polysaccharides, proteins, and extracellular DNA (eDNA), which encases microbial communities. This matrix serves as a protective barrier against environmental stressors, host immune cells, and antibiotic penetration, facilitating chronic and persistent infections (Flemming & Wingender, 2010). Biofilm-forming pathways, such as quorum sensing and cyclic-di-GMP signaling, are the regulatory circuits that coordinate the transition from a free-swimming planktonic state to a sessile, biofilm-associated lifestyle (Miller & Bassler, 2001; Römling et al., 2013). Therapeutic strategies targeting these components aim to either prevent the initial attachment of bacteria or actively disperse established biofilms to enhance the efficacy of conventional antimicrobials. Such interventions are critical in managing infections related to medical implants, cystic fibrosis lung infections, and chronic wounds where traditional antibiotic therapy often fails (Hall & Mah, 2017).
Drugs targeting this system work by degrading extracellular DNA (eDNA) within the matrix, inhibiting quorum sensing (QS) signaling molecules to prevent biofilm maturation, disrupting exopolysaccharide synthesis, or modulating cyclic-di-GMP levels to trigger biofilm dispersal and restore antibiotic sensitivity (Flemming & Wingender, 2010; Römling et al., 2013).
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