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Bacterial surface adhesins and the biofilm matrix are critical structural and functional components that facilitate microbial colonization and persistence within a host [1, 3]. Adhesins are cell-surface proteins or appendages, such as pili, fimbriae, and microbial surface components recognizing adhesive matrix molecules (MSCRAMMs), that mediate the initial attachment of bacteria to host tissues or medical devices [4, 10, 13]. Following attachment, bacteria produce an extracellular polymeric substance (EPS) matrix—composed of polysaccharides, proteins, and extracellular DNA (eDNA)—which provides mechanical stability and protects the community from host immune responses and antibiotic penetration [1, 6, 7]. This protective environment is a hallmark of chronic and device-associated infections, where bacteria exhibit significantly higher tolerance to conventional treatments compared to their planktonic counterparts [2, 14, 17]. Therapeutic strategies targeting these components include anti-adhesion agents that block initial binding, matrix-degrading enzymes that promote biofilm dispersal, and inhibitors of matrix assembly [1, 2, 8, 9]. By disrupting these structures, these therapies aim to transition bacteria back to a vulnerable planktonic state, thereby enhancing the efficacy of standard antimicrobial treatments [2, 16].
Competitive inhibition of adhesin-receptor binding; Enzymatic degradation of matrix components (eDNA, polysaccharides); Inhibition of adhesin assembly or anchoring; Disruption of matrix assembly (anti-assembly)
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