Lipopolysaccharides from Klebsiella pneumoniae (LPS, from bacterial [Klebsiella pneumoniae]) are lipid-polysaccharide endotoxins and TLR4 activators originating from Klebsiella pneumoniae, classified as S-type LPS. They exhibit a characteristic tripartite structure comprising an O-antigen, a core oligosaccharide, and lipid A. These lipopolysaccharides may contribute to bacterial immune evasion by inhibiting complement-mediated killing and suppressing host antimicrobial peptide secretion, thus helping bacteria evade immune defenses. Possessing high viscosity and serum resistance, they can potentially induce sepsis. Additionally, these lipopolysaccharides are utilized in the development of animal models for sepsis/septicemia.

Lipopolysaccharides (LPS) from Klebsiella pneumoniae contribute to the development of sepsis when combined with the bacterium’s capsule polysaccharide (CPS). To maintain LPS integrity, it is recommended to store LPS solutions in silanized containers, as LPS can adhere to plastic and certain types of glass, especially at concentrations below 0.1 mg/mL. This adsorption is minimized when LPS concentrations exceed 1 mg/mL. When using glass containers, ensure thorough mixing for at least 30 minutes before use to dissolve any LPS adsorbed on the tube walls. Intriguingly, the LPS core of Klebsiella pneumoniae lacks the phosphorylated modifications typically found in the core LPS of most Enterobacteriaceae, a unique structure that influences outer membrane permeability and pathogenic mechanisms. Although Lipopolysaccharides and CPS both play roles in sepsis, only CPS is involved in Klebsiella pneumoniae-induced lung infections, as it regulates complement C3 deposition and protects the pathogen from alveolar macrophage-mediated phagocytosis.

Lipopolysaccharides and capsular polysaccharides (CPS) are key virulence factors of Klebsiella pneumoniae, with CPS playing a crucial role in resisting phagocytosis, inhibiting early inflammatory responses, countering antimicrobial peptides, and suppressing dendritic cell maturation. CPS is recommended for use in constructing animal models of disease induction. In a mouse hyperglycemia model, lipopolysaccharides from Klebsiella pneumoniae (0.05 μg per animal; intratracheal instillation) decrease pulmonary granulocyte recruitment, reduce early production of CXCL1, CXCL2, IL-1β, and TNF-α, and inhibit the expression of TLR2 and TIRAP. These characteristics further increase susceptibility to K. pneumoniae infections.