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Bacterial surface macromolecules and biofilm extracellular polymeric substances (EPS) represent the complex structural components that define the bacterial cell boundary and the protective matrix of microbial communities. Surface macromolecules, including peptidoglycan, lipopolysaccharides (LPS), and teichoic acids, are essential for maintaining cell shape and mediating interactions with the host immune system (Silhavy et al., 2010). EPS is a self-produced mixture of polysaccharides, extracellular DNA (eDNA), proteins, and lipids that forms the scaffold of biofilms, providing a physical barrier against antibiotics and host defenses (Flemming & Wingender, 2010). These structures play a pivotal role in the pathogenesis of chronic infections, such as those associated with cystic fibrosis and medical device colonization, by facilitating persistent survival and antimicrobial tolerance. Therapeutic interventions targeting these components often involve biofilm-dispersing agents like DNases or glycoside hydrolases that degrade the EPS matrix, or membrane-active antibiotics that bind to surface lipids (Tetz et al., 2009). By destabilizing the biofilm architecture or the bacterial envelope, these treatments aim to restore the efficacy of conventional antimicrobials and promote pathogen clearance.
Drugs targeting these components act through enzymatic degradation of the extracellular matrix (e.g., DNases, glycoside hydrolases), physical disruption of the bacterial surface via detergent-like effects (e.g., polymyxins), or inhibition of the biosynthetic pathways for matrix polymers (Flemming & Wingender, 2010; StatPearls).
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