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

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 Acute Lung Injury Model^[1][2].
It is recommended to prepare a solution with concentration ≥2 mg/mL. Vortex thoroughly for more than 10 minutes. Due to the adsorption characteristics of LPS, silanized container or low adsorption centrifuge tubes should be used for aliquoting and storage, and mix thoroughly before use.

TLR-4^[2]

Note:
1. Concentration and Time: Please do not rely solely on a single article to determine experimental conditions. It is recommended to review relevant literature based on the cell line and type of LPS before formal experiments, as the required induction time or optimal concentration for different inflammatory factors to reach their peak may vary. It is advisable to set concentration and time gradients to identify the optimal experimental scheme.
2. Detection Indicators: LPS does not necessarily induce cell death; therefore, it is not appropriate to determine the LPS modeling concentration and time solely by assessing cell viability. It is recommended to measure the expression or secretion of inflammatory factors.
3. Solvent Selection: Literature indicates that certain concentrations of DMSO can significantly inhibit LPS-induced inflammatory responses. In cellular experiments, it is recommended to prepare stock solutions using sterile water, followed by dilution with culture medium.
4. Container Selection: Due to the adsorption characteristics of LPS, it can bind to plastics and certain types of glass (especially at concentrations <0.1 mg/mL). The adsorption effect is relatively small when LPS concentrations exceed 1 mg/mL. Additionally, LPS tends to form micelles in solution. Therefore, when dissolving the powder, it is recommended to prepare concentrations of ≥2 mg/mL, and to vortex thoroughly for more than 10 minutes. If necessary, ultrasonic assistance may be used. For storage, please use silanized containers or low-adhesion centrifuge tubes. If glass containers are used, ensure to mix thoroughly for at least 30 minutes prior to use to re-dissolve any LPS adsorbed to the wall of the container.
5. Concentration Units: LPS does not have a uniform molecular weight because its molecules exhibit heterogeneity and aggregation. The molecular weight of naturally sourced LPS typically ranges from 10-100 kDa or even higher. Common dosing concentrations for LPS found in the literature are in terms of mass concentration, such as ng/mL and μg/mL, so it is sufficient to prepare solutions directly in mass concentration during experiments.
6. Filtration Sterilization: After dissolving LPS powder in water, saline, or PBS, the solution may appear turbid or colloidal, and in some cases, a microsphere distribution with diameters around 20-30 nm may be observed. When sterilizing by filtration, do not filter the stock solution directly. It is recommended to dilute to working solution first and then filter sterilize through a 0.22 μm filter membrane.
7. Differences Among Different Strain LPS: LPS of different catalog numbers comes from various bacterial strains, corresponding to different structural features such as lipid A, core polysaccharides, and O-antigens, which in turn affect the intensity of inflammation induction and TLR4-mediated signaling bias. Commonly referenced LPS catalog numbers for in vitro or in vivo inflammation model construction include HY-D1056 and HY-D1056A1. Moreover, in specific research contexts, specialized sources of LPS related to the studied bacterial strains may also be used. For example, HY-D1056D (from Porphyromonas gingivalis) is used in periodontal studies, while HY-D1056B3 (from Klebsiella pneumoniae) is relevant in pneumonia-related research. When selecting LPS, considerations should include the purpose of the experiment, sensitivity of the cell line, and other factors.

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* 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.

Solid

White to off-white

[Lipopolysaccharides, from Klebsiella pneumoniae]

Room temperature in continental US; may vary elsewhere.

• [1]. Izquierdo L, et al. The Klebsiella pneumoniae wabG gene: role in biosynthesis of the core lipopolysaccharide and virulence. J Bacteriol. 2003 Dec;185(24):7213-21.  [Content Brief]

  [2]. Li B, Zhao Y, Liu C, Chen Z, Zhou D. Molecular pathogenesis of Klebsiella pneumoniae. Future Microbiol. 2014;9(9):1071-81.  [Content Brief]

  [3]. Martinez N, Ketheesan N, Martens GW, West K, Lien E, Kornfeld H. Defects in early cell recruitment contribute to the increased susceptibility to respiratory Klebsiella pneumoniae infection in diabetic mice. Microbes Infect. 2016 Oct;18(10):649-655.  [Content Brief]