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Klebsiella pneumoniae capsular polysaccharide (CPS) antigens, specifically serotypes K1 and K2, are the primary virulence factors of hypervirulent K. pneumoniae (hvKP) strains [1, 2]. These polysaccharides form a thick, mucoid layer on the bacterial surface that protects the pathogen from host immune defenses by inhibiting phagocytosis and resisting complement-mediated killing [3, 4]. Serotypes K1 and K2 are most frequently associated with severe, invasive community-acquired infections, such as pyogenic liver abscesses, meningitis, and endophthalmitis, often in otherwise healthy individuals [1, 5]. The K1 serotype is particularly linked to the ST23 sequence type, while K2 is found across various sequence types including ST25, ST65, and ST86 [2, 15]. Because of their critical role in pathogenesis and high prevalence in invasive disease, these antigens are major targets for the development of glycoconjugate vaccines and monoclonal antibodies [6, 9]. Experimental vaccines, often utilizing phage-derived depolymerases to create immunogenic oligosaccharides conjugated to carrier proteins like CRM197, have shown promise in inducing protective, serotype-specific bactericidal antibodies [6, 12]. Passive immunotherapy using monoclonal antibodies targeting these specific CPS types is also being explored as a treatment for severe infections [1, 11]. Targeting these antigens provides a potential alternative or adjunct to traditional antibiotic therapy, especially in the context of rising multidrug resistance in Klebsiella species [8, 10].
Induction of opsonophagocytic and bactericidal antibodies; Neutralization of capsular virulence; Promotion of complement-mediated killing [1, 6].
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