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Microbial biofilms are complex, multicellular communities of microorganisms embedded within a self-produced extracellular polymeric substance (EPS) matrix, which is composed of polysaccharides, proteins, and extracellular DNA [1, 2, 4]. This structural arrangement serves as a formidable protective barrier, allowing microbes to withstand environmental stressors, host immune defenses, and antimicrobial treatments [8, 11]. In clinical settings, biofilms are a leading cause of chronic and persistent infections, particularly those associated with indwelling medical devices such as catheters, heart valves, and orthopedic implants [10, 15]. The resistance of biofilm-encapsulated bacteria to antibiotics can be 100 to 1,000 times higher than that of their planktonic counterparts, necessitating novel therapeutic approaches [4, 6, 9]. Current drug development strategies target various stages of the biofilm life cycle, including initial adhesion, quorum sensing-mediated communication, and the integrity of the EPS matrix itself [1, 7, 14]. Disrupting these structures using matrix-degrading enzymes or signaling inhibitors can restore antibiotic susceptibility and aid in the clearance of recalcitrant infections [1, 2, 13].
Degradation of the extracellular polymeric substance matrix, inhibition of quorum sensing (quorum quenching), prevention of initial bacterial adhesion, and enhancement of antimicrobial penetration through structural disruption [1, 2, 4, 6].
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