3-deoxy-D-manno-octulosonic acid (Kdo2-Lipid A) is the essential component of lipopolysaccharide in most Gram-negative bacteria and the minimal structural component to sustain bacterial viability. It serves as the active component of lipopolysaccharide to stimulate potent host immune responses through the complex of Toll-like-receptor 4 (TLR4) and myeloid differentiation protein 2 (MD2). Therefore, Kdo2-lipid A is an important stimulator for studying the mechanism of the innate immune system and for developing bacterial vaccine adjuvants. Kdo2 Lipid A/TLR4 antagonists can also be applied in anti-inflammatory interventions. Kdo2-lipid A, induces de novo sphingolipid biosynthesis in RAW264.7 macrophages, which is essential for induction of autophagy. Kdo2-Lipid A has been used in animal atherosclerosis model.
Other Notes
Solubility: Kdo2 -Lipid A can be dissolved in a solution of 0.1-0.5% Triethylamine (Sigma Cat# 90335) at 1 mg/ml (In case of percipitation use sonication). Use sonication to directly solublized in cell culture medium. Storage: Once Kdo2-lipidA is dissolved in 0.1-0.5% Triethylamine (Sigma Cat# 90335) aliquot and store at -20°C. The solution is stable for 2 months in -20°C.
The Journal of biological chemistry, 285(49), 38568-38579 (2010-09-30)
Activation of RAW264.7 cells with a lipopolysaccharide specific for the TLR4 receptor, Kdo(2)-lipid A (KLA), causes a large increase in cellular sphingolipids, from 1.5 to 2.6 × 10(9) molecules per cell in 24 h, based on the sum of subspecies
Oxidized low-density lipoprotein (LDL) is an important determinant of inflammation in atherosclerotic lesions. It has also been documented that certain chronic infectious diseases, such as periodontitis and chlamydial infection, exacerbate clinical manifestations of atherosclerosis. In addition, low-level but persistent metabolic
Inflammation and macrophage foam cells are characteristic features of atherosclerotic lesions, but the mechanisms linking cholesterol accumulation to inflammation and LXR-dependent response pathways are poorly understood. To investigate this relationship, we utilized lipidomic and transcriptomic methods to evaluate the effect
Journal of lipid research, 47(5), 1097-1111 (2006-02-16)
The LIPID MAPS Consortium (www.lipidmaps.org) is developing comprehensive procedures for identifying all lipids of the macrophage, following activation by endotoxin. The goal is to quantify temporal and spatial changes in lipids that occur with cellular metabolism and to develop bioinformatic
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