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Klebsiella pneumoniae surface polysaccharide refers mainly to two major classes of surface-exposed carbohydrate polymers: the capsular polysaccharide (CPS, or K-antigen) and the O-antigen of lipopolysaccharide (LPS). The CPS forms a thick, protective capsule around the bacterium, composed of diverse repeating oligosaccharide units, and is one of the primary determinants of immune evasion, serum resistance, and virulence in K. pneumoniae. The O-antigen is the distal portion of LPS and contributes additional serotype diversity and immune evasion mechanisms. Both CPS and O-antigen are major targets for the development of vaccines, antibody therapies, and bacteriophage-based therapies. The antigenic diversity, especially for the capsule, presents a key challenge for broad-spectrum targeting, but these surface polysaccharides remain critical to bacterial survival, pathogenesis, and therapeutic targeting in drug-resistant and hypervirulent strains[1][2][4][6][7][8]. - The capsule (CPS) is the most important virulence factor and enables K. pneumoniae to resist phagocytosis and complement-mediated killing[1][3][6]. - Both CPS and O-antigen exhibit high structural variability, defining the serotype and affecting virulence and susceptibility to drugs, antibodies, and phages[1][2][7]. - Therapies targeting these polysaccharides include investigational CPS-based vaccines, monoclonal antibodies, and phage therapies; no approved CPS-based vaccines exist as of 2025[6][8]. - Surface polysaccharide expression and structure also correlate with biofilm formation, another key virulence trait complicating infections[5]. - This diversity and adaptability are at the core of K. pneumoniae's ability to cause serious, drug-resistant hospital-acquired infections.
Disruption of capsule integrity (e.g., by cationic peptides such as polymyxins)[4] Neutralization or opsonization by antibodies for enhanced immune clearance[6][8] Bacteriophage lysis by binding/recognizing surface polysaccharide antigens[2]
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