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Bacterial biofilm and adhesion machinery refers to the complex assembly of proteins, polysaccharides, and extracellular DNA (eDNA) that enables bacteria to attach to surfaces and form resilient, multicellular communities [1, 2]. This machinery includes cell-surface adhesins, such as pili and fimbriae, and the extracellular polymeric substances (EPS) that constitute the biofilm matrix [4, 5]. These structures play a critical role in the pathogenesis of chronic and healthcare-associated infections by protecting bacteria from host immune responses and increasing their tolerance to antibiotics by up to 1000-fold [3, 10]. Therapeutic strategies targeting this machinery aim to prevent initial colonization, degrade the protective matrix, or trigger biofilm dispersal to restore antibiotic sensitivity [1, 5]. Drugs interacting with these targets include matrix-degrading enzymes like dornase alfa (DNase I) and dispersin B, as well as small-molecule inhibitors of adhesins and quorum-sensing pathways [1, 4]. Despite their potential, challenges include the risk of systemic bacterial spread during dispersal and the need for high local concentrations to penetrate established biofilms [2, 10].
Inhibition of bacterial attachment, degradation of extracellular matrix, disruption of quorum sensing, and induction of biofilm dispersal [1, 2, 4].
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