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Bacterial biofilms are complex, sessile communities of microorganisms characterized by cells that are irreversibly attached to a substratum or interface and embedded in a self-produced matrix of extracellular polymeric substances (EPS) (Donlan, 2002). This matrix, composed of polysaccharides, proteins, and extracellular DNA (eDNA), serves as a physical and chemical barrier that protects bacteria from environmental stressors, host immune cells, and antimicrobial therapy (Flemming & Wingender, 2010). The cell surfaces within the biofilm are often modified to enhance adhesion and facilitate the structural stability of the community (Karygianni et al., 2020). Targeting these structures is essential for treating chronic infections, such as those associated with cystic fibrosis or indwelling medical devices, where traditional antibiotics often fail due to poor penetration (Ciofu et al., 2022). Therapeutic strategies involve the use of matrix-degrading enzymes, such as DNases and glycoside hydrolases, or small molecules that interfere with the signaling pathways regulating biofilm formation (Roy et al., 2018). By destabilizing the matrix and the cell surface interactions, these treatments aim to restore antibiotic susceptibility and promote the clearance of the infection by the host (Hall-Stoodley et al., 2004).
Degradation of extracellular DNA and polysaccharides, chelation of stabilizing metal ions, inhibition of bacterial adhesion, and disruption of the cell envelope to enhance antibiotic penetration (Roy et al., 2018; Flemming & Wingender, 2010).
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