Lipopolysaccharides from Escherichia coli O111:B4
(Synonyms: LPS, 脂多糖) 目录号 : GC19203
从大肠杆菌O111:B4中提取，并通过凝胶过滤纯化
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
| Cell experiment [1]: | |
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Cell lines |
Human cancer cell line HT-29 |
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Preparation Method |
HT-29 cells were incubated at 37℃ in a humidified atmosphere of 5% CO2 in low-D-glucose (16.67 mM) McCoy's 5a Medium Modified supplemented with 10% v/v heat-inactivated FBS, 2 mM L-glutamine, and 1% penicillin/streptomycin. |
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Reaction Conditions |
Prior to any treatment, cells were allowed to reach confluence in plate wells, and then monolayers were exposed to a range of concentrations of carrageenans (10, 50, and 100 μg x mL–1, final value), lipopolysaccharides (10 μg x mL–1, final value). Furthermore, stress model was induced by ethanol (10%). |
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Applications |
Mixtures of lipopolysaccharides and carrageenans exhibited a tendency toward the reference profile not exposed to ethanol, but at a rate less rapid than that of cells preincubated with the carrageenan alone. In the presence of lipopolysaccharides, κ/β-carrageenan remained active, whereas the other carrageenans had no activity. The differences. |
| Animal experiment [2]: | |
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Animal models |
Male Sprague-Dawley rats (200 – 250 g) |
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Preparation Method |
Animals were housed with free access to food and water. Lipopolysaccharide from Salmonella thyphosa (Sigma) dissolved in endotoxin-free saline was used for intraperitoneal injection. Animals were sacrificed after 2, 6, 12, and 24 h, and pancreas, liver, kidney, lung, brain, and intestine were processed. |
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Dosage form |
30 mg/kg |
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Applications |
Lipopolysaccharide treatment could induce p8 mRNA expression in the pancreas. Maximal induction (31fold) was observed after 12 h and expression remained significantly elevated after 24 h. p8 mRNA was also overexpressed after Lipopolysaccharide intraperitoneal injection in liver and kidney. Maximal p8 mRNA expression was obtained after 6 and 12 h of the LPS treatment in kidney and liver respectively. Induction was of 10 and 8fold in liver and kidney respectively. |
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References: [1]. Sokolova EV, et al. Effect of carrageenans alone and in combination with casein or lipopolysaccharide on human epithelial intestinal HT-29 cells. J Biomed Mater Res A. 2017 Oct;105(10):2843-2850. [2]. Jiang YF, et al. Lipopolysaccharides induce p8 mRNA expression in vivo and in vitro. Biochem Biophys Res Commun. 1999 Jul 14;260(3):686-90. |
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This product is extracted from E. coli serotype O111:B4 and purified by gel filtration. The source strain is from a private collection. This LPS serotype has been used to stimulate B-cells and induce NOS in human hepatocytes.
Lipopolysaccharides (LPSs) are characteristic components of the cell wall of Gram-negative bacteria. LPS and its lipid A moiety stimulate cells of the innate immune system by the Toll-like receptor 4 (TLR4), a member of the Toll-like receptor protein family, which recognizes common pathogen-associated molecular-patterns (PAMPs).
Lipopolysaccharide (LPS) is vital to both the structural and functional integrity of the Gram-negative bacterial outer membrane. Ubiquitously expressed by all Gram-negative bacteria, and containing several well-conserved domains, lipopolysaccharide also serves as one of the primary targets of the innate arm of the mammalian immune system. The lipopolysaccharides have a profound effect on the mammalian immune system and are of great significance in the pathophysiology of many disease processes.[1]
In vitro study indicated that the bone resorption and the inhibition of collagen synthesis caused by lipopolysaccharide could be prevented by PB effectively. Lipopolysaccharide at a concentration of 10μg /ml inhibited bone collagen synthesis by 43% and PB reversed this inhibition in a dose-dependent manner. Even at concentrations as low as 5 μg/ml (PB: LPS =1:2) it reduced the bone-resorbing activity of the lipopolysaccharide by 85%. This effect was specific for resorption stimulated by lipopolysaccharide.[2]
Lipopolysaccharide preconditioning to mice obviously reduced coelenterazine-Induced fluorescent lesions of Colon26 cells at 7 and 14 days after the intraportal inoculation of Colon26 cells, which expressed Nano-lantern, in comparison to control mice. Moreover, lipopolysaccharide preconditioning significantly reduced the fluorescence intensity of tumors than that of the control mice at both 7 and 14 days after tumor inoculation as well as reduced the liver weight in comparison to control mice at 14 days. Results showed that tumor metastasis was exclusively found in the lungs but not liver. Lipopolysaccharide preconditioning also tended to reduce lung metastasis in vivo.[3]
这个产品是从大肠杆菌O111:B4中提取的，并通过凝胶过滤纯化。源菌株来自私人收藏。这种LPS血清型已被用于刺激B细胞并在人类肝细胞中诱导NOS。
脂多糖（LPS）是革兰氏阴性菌细胞壁的特征成分。LPS及其脂质A部分通过Toll样受体4（TLR4）刺激先天免疫系统中的细胞，TLR4是Toll样受体蛋白家族的一员，可以识别常见的病原相关分子模式（PAMPs）。
脂多糖（LPS）对于革兰氏阴性细菌的外膜结构和功能完整性至关重要。所有革兰氏阴性细菌都广泛表达LPS，并包含几个保守区域，因此LPS也是哺乳动物先天免疫系统主要攻击目标之一。 LPS对哺乳动物免疫系统有深远影响，在许多疾病过程中具有重要意义。[1]
实验室研究表明，PB可以有效地预防脂多糖引起的骨吸收和胶原合成抑制。浓度为10μg/ml的脂多糖可将骨胶原合成抑制43％，而PB则以剂量依赖方式逆转了这种抑制作用。即使在低至5 μg/ml（PB：LPS = 1:2）的浓度下，它也能将脂多糖引起的骨吸收活性降低85％。这种效应是特异性针对由脂多糖刺激引起的吸收现象。
给小鼠进行脂多糖预处理后，与对照组相比，在肝门注射Nano-lantern标记的Colon26细胞后7天和14天时，明显减少了Coelenterazine诱导的荧光损伤。此外，脂多糖预处理还显著降低了肿瘤在7天和14天时的荧光强度，并且在第14天减轻了肝重量。结果显示，只有肺部出现了转移性肿瘤而没有发现在肝内。同时，在体内也倾向于减少肺部转移。
References:
[1]. Erridge C, et al. Structure and function of lipopolysaccharides. Microbes Infect. 2002 Jul;4(8):837-51.
[2]. Harvey W, et al. In vitro inhibition of lipopolysaccharide-induced bone resorption by polymyxin B. Br J Exp Pathol. 1986 Oct;67(5):699-705.
[3]. Nishikawa M, et al. Lipopolysaccharide preconditioning reduces liver metastasis of Colon26 cells by enhancing antitumor activity of natural killer cells and natural killer T cells in murine liver. J Gastroenterol Hepatol. 2021 Jul;36(7):1889-1898.
| Cas No. | SDF | ||
| 别名 | LPS, 脂多糖 | ||
| 分子式 | 分子量 | ||
| 溶解度 | Soluble in water (5 mg/ml) or cell culture medium (1 mg/ml) | 储存条件 | -20℃ |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
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| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
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2.
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Biosynthesis and export of bacterial lipopolysaccharides
Annu Rev Biochem2014;83:99-128.PMID: 24580642DOI: 10.1146/annurev-biochem-060713-035600
lipopolysaccharides molecules represent a unique family of glycolipids based on a highly conserved lipid moiety known as lipid A. These molecules are produced by most gram-negative bacteria, in which they play important roles in the integrity of the outer-membrane permeability barrier and participate extensively in host-pathogen interplay. Few bacteria contain lipopolysaccharides molecules composed only of lipid A. In most forms, lipid A is glycosylated by addition of the core oligosaccharide that, in some bacteria, provides an attachment site for a long-chain O-antigenic polysaccharide. The complexity of lipopolysaccharides structures is reflected in the processes used for their biosynthesis and export. Rapid growth and cell division depend on the bacterial cell's capacity to synthesize and export lipopolysaccharides efficiently and in large amounts. We review recent advances in those processes, emphasizing the reactions that are essential for viability.
Challenges of using lipopolysaccharides for cancer immunotherapy and potential delivery-based solutions thereto
Ther Deliv2019 Mar;10(3):165-187.PMID: 30909855DOI: 10.4155/tde-2018-0076
Despite being one of the earliest Toll-like receptor (TLR)-based cancer immunotherapeutics discovered and investigated, the full extent of lipopolysaccharides (LPS) potentials within this arena remains hitherto unexploited. In this review, we will debate the challenges that have complicated the improvement of LPS-based immunotherapeutic approaches in cancer therapy. Based on their nature, those will be discussed with a focus on side effect-related, tolerance-related and in vivo model-related challenges. We will then explore how drug delivery strategies can be integrated within this domain to address such challenges in order to improve the therapeutic outcome, and will present a summary of the studies that have been dedicated thereto. This paper may inspire further developments based on reconciling the advantages of drug delivery and LPS-based cancer immunotherapy.
lipopolysaccharides in diazotrophic bacteria
Front Cell Infect Microbiol2014 Sep 3;4:119.PMID: 25232535DOI: 10.3389/fcimb.2014.00119
Biological nitrogen fixation (BNF) is a process in which the atmospheric nitrogen (N2) is transformed into ammonia (NH3) by a select group of nitrogen-fixing organisms, or diazotrophic bacteria. In order to furnish the biologically useful nitrogen to plants, these bacteria must be in constant molecular communication with their host plants. Some of these molecular plant-microbe interactions are very specific, resulting in a symbiotic relationship between the diazotroph and the host. Others are found between associative diazotrophs and plants, resulting in plant infection and colonization of internal tissues. Independent of the type of ecological interaction, glycans, and glycoconjugates produced by these bacteria play an important role in the molecular communication prior and during colonization. Even though exopolysaccharides (EPS) and lipochitooligosaccharides (LCO) produced by diazotrophic bacteria and released onto the environment have their importance in the microbe-plant interaction, it is the lipopolysaccharides (LPS), anchored on the external membrane of these bacteria, that mediates the direct contact of the diazotroph with the host cells. These molecules are extremely variable among the several species of nitrogen fixing-bacteria, and there are evidences of the mechanisms of infection being closely related to their structure.
lipopolysaccharides: Biosynthetic pathway and structure modification
Prog Lipid Res2010 Apr;49(2):97-107.PMID: 19815028DOI: 10.1016/j.plipres.2009.06.002
lipopolysaccharides that constitutes the outer leaflet of the outer membrane of most Gram-negative bacteria is referred to as an endotoxin. It is comprised of a hydrophilic polysaccharide and a hydrophobic component referred to as lipid A. Lipid A is responsible for the major bioactivity of endotoxin, and is recognized by immune cells as a pathogen-associated molecule. Most enzymes and genes coding for proteins responsible for the biosynthesis and export of lipopolysaccharides in Escherichia coli have been identified, and they are shared by most Gram-negative bacteria based on genetic information. The detailed structure of lipopolysaccharides differs from one bacterium to another, consistent with the recent discovery of additional enzymes and gene products that can modify the basic structure of lipopolysaccharides in some bacteria, especially pathogens. These modifications are not required for survival, but are tightly regulated in the cell and closely related to the virulence of bacteria. In this review we discuss recent studies of the biosynthesis and export of lipopolysaccharides, and the relationship between the structure of lipopolysaccharides and the virulence of bacteria.
Recognition of lipopolysaccharides pattern by TLR4 complexes
Exp Mol Med2013 Dec 6;45(12):e66.PMID: 24310172DOI: 10.1038/emm.2013.97
lipopolysaccharides (LPS) is a major component of the outer membrane of Gram-negative bacteria. Minute amounts of LPS released from infecting pathogens can initiate potent innate immune responses that prime the immune system against further infection. However, when the LPS response is not properly controlled it can lead to fatal septic shock syndrome. The common structural pattern of LPS in diverse bacterial species is recognized by a cascade of LPS receptors and accessory proteins, LPS binding protein (LBP), CD14 and the Toll-like receptor4 (TLR4)-MD-2 complex. The structures of these proteins account for how our immune system differentiates LPS molecules from structurally similar host molecules. They also provide insights useful for discovery of anti-sepsis drugs. In this review, we summarize these structures and describe the structural basis of LPS recognition by LPS receptors and accessory proteins.