Lipopolysaccharides, from Klebsiella pneumoniae

Lipopolysaccharides, from Klebsiella pneumoniae (LPS, from bacterial (Klebsiella pneumoniae)) is a lipopolysaccharide endotoxin and TLR4 activator derived from Klebsiella pneumoniae, belonging to the S-type LPS. Lipopolysaccharides, from Klebsiella pneumoniae possesses a typical three-part structure: O-antigen, core oligosaccharide, and lipid A. Lipopolysaccharides, from Klebsiella pneumoniae may play a role in bacterial immune evasion by inhibiting complement-mediated killing and host antimicrobial peptide secretion, enabling bacteria to evade immune defense. Lipopolysaccharides, from Klebsiella pneumoniae exhibits high viscosity and anti-serum killing properties, and may induce sepsis. Lipopolysaccharides, from Klebsiella pneumoniae is commonly used to construct animal sepsis models.

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.

Method: Streptozotocin-induced hyperglycemic mice and control mice received Klebsiella pneumoniae lipopolysaccharide by intratracheal instillation at 0.05 μg per mouse, and early pulmonary inflammatory responses were measured. Result: Compared with non-diabetic controls exposed to the same LPS, hyperglycemic mice showed reduced granulocyte recruitment and lower early CXCL1, CXCL2, IL-1β, and TNF-α responses, together with reduced TLR2 and TIRAP expression. This represents impaired host responsiveness in diabetes rather than an intrinsic anti-inflammatory action of LPS.^[1]