2. Immunology/Inflammation
  3. Toll-like Receptor (TLR)
  4. Lipopolysaccharides, from Klebsiella pneumoniae

Lipopolysaccharides, from Klebsiella pneumoniae  (Synonyms: LPS, from bacterial (Klebsiella pneumoniae))

Cat. No.: HY-D1056B3
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Lipopolysaccharides, from Klebsiella pneumoniae (LPS, from bacterial (Klebsiella pneumoniae)) are lipopolysaccharide endotoxins and TLR4 activators derived from Klebsiella pneumoniae, and are classified as S-type LPS. Lipopolysaccharides, from Klebsiella pneumoniae exhibit a typical three-part structure: O-antigen, core oligosaccharide, and lipid A. Lipopolysaccharides, from Klebsiella pneumoniae may participate in bacterial immune evasion by inhibiting complement-mediated killing and suppressing the host's secretion of antimicrobial peptides, thereby allowing the bacteria to escape immune defenses. Lipopolysaccharides, from Klebsiella pneumoniae possess high viscosity and resistance to serum-mediated killing, which may lead to sepsis. Lipopolysaccharides, from Klebsiella pneumoniae can be used to construct animal models of sepsis.

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Lipopolysaccharides, from Klebsiella pneumoniae Chemical Structure

Lipopolysaccharides, from Klebsiella pneumoniae Chemical Structure

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Lipopolysaccharides, from Klebsiella pneumoniae Related Antibodies

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Description

Lipopolysaccharides, from Klebsiella pneumoniae (LPS, from bacterial (Klebsiella pneumoniae)) are lipopolysaccharide endotoxins and TLR4 activators derived from Klebsiella pneumoniae, and are classified as S-type LPS. Lipopolysaccharides, from Klebsiella pneumoniae exhibit a typical three-part structure: O-antigen, core oligosaccharide, and lipid A. Lipopolysaccharides, from Klebsiella pneumoniae may participate in bacterial immune evasion by inhibiting complement-mediated killing and suppressing the host's secretion of antimicrobial peptides, thereby allowing the bacteria to escape immune defenses. Lipopolysaccharides, from Klebsiella pneumoniae possess high viscosity and resistance to serum-mediated killing, which may lead to sepsis. Lipopolysaccharides, from Klebsiella pneumoniae can be used to construct animal models of sepsis[1][2].

IC50 & Target

TLR-4[2]
In Vitro

Note:
To maintain the integrity of LPS, it is recommended to store LPS solution in silanized containers. This is because LPS can adhere to plastics and certain types of glass, particularly at concentrations below 0.1 mg/mL. If the LPS concentration exceeds 1 mg/mL, this adsorption effect is relatively minimal. If using glass containers, ensure that the solution is thoroughly mixed for at least 30 minutes before use to redissolve any LPS that may have adsorbed to the tube walls.

The lipopolysaccharide of Klebsiella pneumoniae can replace l,d-HeppII with an α-d-galacturonic acid (α-d-GalpA) residue at the O-3 position. In most studied Enterobacteriaceae, the core LPS contains phosphorylation modifications in the inner core, but the core LPS of Klebsiella pneumoniae lacks this modification. This unique core structure determines the outer membrane permeability and specific pathogenesis of Klebsiella pneumoniae[1].
Lipopolysaccharides, from Klebsiella pneumoniae, together with bacterial capsular polysaccharide (capsule polysaccharide, CPS), promote the development of sepsis. However, only CPS is involved in Klebsiella pneumoniae-induced pulmonary infections because only CPS regulates the deposition of complement C3 and protects the pathogen from alveolar macrophage-mediated phagocytosis[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Lipopolysaccharides, from Klebsiella pneumoniae Related Antibodies
In Vivo

Lipopolysaccharides, from *Klebsiella pneumoniae* and capsular polysaccharide (CPS) are both important virulence factors of *Klebsiella pneumoniae*, while CPS plays a crucial role in anti-phagocytosis, inhibiting early inflammatory responses, resisting antimicrobial peptides, and suppressing dendritic cell maturation. It is recommended to use PCS together to construct animal disease induction models[2].
Lipopolysaccharides, from *Klebsiella pneumoniae* (0.05 μg/animal; intratracheal instillation) reduce pulmonary granulocyte recruitment, decrease the early production of CXCL1, CXCL2, IL-1β, and TNF-α, and suppress the expression of TLR2 and TIRAP in a mouse hyperglycemia model. This characteristic further increases susceptibility to *Klebsiella pneumoniae* infection[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Male C57BL/6 mice, streptozotocin-induced diabetes mouse model[3]
Dosage: 0.05 μg of Klebsiella pneumoniae LPS in 50 μL of PBS
Administration: Tracheal instillation
Result: Resulted a significant reduction in survival compared to control mice after tracheal instillation of Klebsiella pneumoniae.
Induced recruitement of fewer granulocytes to the alveolar airspace and reduced early production of CXCL1, CXCL2, IL-1β and TNF-α following tracheal instillation of Klebsiella pneumoniae-lipopolysaccharide.
Additionally, decreased TLR2 and TIRAP expression following in hyperglycemic mice.
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Solid

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White to off-white

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[Lipopolysaccharides, from Klebsiella pneumoniae]
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Room temperature in continental US; may vary elsewhere.
Storage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
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In Vitro: 

H2O : 5 mg/mL (Need ultrasonic and warming)

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Lipopolysaccharides, from Klebsiella pneumoniae Related Classifications

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Lipopolysaccharides, from Klebsiella pneumoniaeLPS, from bacterial (Klebsiella pneumoniae)Toll-like Receptor (TLR)Inhibitorinhibitorinhibit

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