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Alginate exopolysaccharide of Pseudomonas aeruginosa is a high molecular weight, linear copolymer of β-D-mannuronic acid and α-L-guluronic acid secreted by P. aeruginosa, especially under stress or in chronic lung infections such as those seen in cystic fibrosis patients[1][2][4][5]. It serves as the main component of the extracellular matrix in mucoid biofilms, providing a protective barrier against antibiotics, host immune defenses, and environmental challenges[4][5]. Alginate promotes strong biofilm formation and adherence to various surfaces, enabling persistence, chronic infection, and antibiotic resistance[1][2][4]. Clinical interest surrounds alginate as a therapeutic target due to its key role in chronic infections and biofilm stability; approaches such as alginate lyase enzymes are being researched to disrupt biofilms and enhance the efficacy of antimicrobial therapies[4][6]. While most environmental and early clinical isolates do not overproduce alginate, its overproduction (mucoid phenotype) is a hallmark of late-stage, difficult-to-treat P. aeruginosa infections, especially in cystic fibrosis and chronic wound patients[9].
Enzymatic degradation (alginate lyase disrupts the protective biofilm matrix by cleaving the exopolysaccharide, promoting bacterial clearance) Agents that inhibit alginate biosynthesis (theoretical, experimental), interfere with protective matrix formation
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