Lipopolysaccharides from Escherichia coli O111:B4 |
| (Synonyms: LPS) Catalog No.: GC19203 |
Extracted from E. coli serotype O111:B4 and purified by gel filtration.
Products are for research use only. Not for human use. We do not sell to patients.
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
| Cell experiment [1]: | |
|
Cell lines |
Human cancer cell line HT-29 |
|
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. |
|
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%). |
|
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]: | |
|
Animal models |
Male Sprague-Dawley rats (200 – 250 g) |
|
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. |
|
Dosage form |
30 mg/kg |
|
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. |
|
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. |
|
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]
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 | ||
| Synonyms | LPS | ||
| Formula | M.Wt | ||
| Solubility | Soluble in water (5 mg/ml) or cell culture medium (1 mg/ml) | Storage | Store at 2-8°C |
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. | ||
| Shipping Condition | Evaluation sample solution : ship with blue ice All other available size: ship with RT , or blue ice upon request |
||
Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)
g
μL
Step 2: Enter the in vivo formulation (This is only the calculator, not formulation. Please contact us first if there is no in vivo formulation at the solubility Section.)
Calculation results:
Working concentration: mg/ml;
Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )
Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL saline, mix and clarify.
Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.
Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such as vortex, ultrasound or hot water bath can be used to aid dissolving.
3. All of the above co-solvents are available for purchase on the GlpBio website.
Oral administration of lipopolysaccharides from Escherichia coli (serotype O111:B4) does not induce an effective systemic immune response in milk-fed Holstein calves
It is well established that intravenous administration of lipopolysaccharides (LPS)-cell wall components from gram-negative bacteria-induce acute inflammatory responses in dairy calves, but the effect of oral administration of LPS to dairy calves is currently unknown. To evaluate the effects of oral administration of LPS derived from Escherichia coli (serotype O111:B4) on innate immune responses in milk-fed Holstein calves, 20 visually healthy calves (34 ± 1 d) received 4 L of milk with LPS (12 μg/kg body weight; n = 10; LPS) or without LPS (n = 10; control) at the morning feeding. Samples were collected at 0.5 h before the morning feeding and at 3, 6, 24, 48, 72, and 168 h after the morning feeding to measure rectal temperature and heart rate, as well as plasma-negative and plasma-positive acute phase proteins (i.e., haptoglobin, serum amyloid A, albumin, total protein, and fibrinogen) and immunoglobulin concentrations (IgG, IgM, and IgA). None of these measurements was affected by the oral administration of LPS. Oral administration of LPS at 12 μg/kg of body weight did not induce an acute inflammatory response in visually healthy milk-fed Holstein calves when administered in milk.
Immunometabolic Endothelial Phenotypes: Integrating Inflammation and Glucose Metabolism
[Figure: see text].
Inhibition of glycolysis alleviates lipopolysaccharide-induced acute lung injury in a mouse model
Gluconic metabolic reprogramming, immune response, and inflammation are intimately linked. Glycolysis involves in the pathologic progress in acute and chronic inflammatory diseases. However, the involvement of glycolysis in the acute lung injury (ALI) is still unclear. This study investigated the role of glycolysis in an animal model of ALI. First, we found that lactate content in serum was remarkably increased in ALI patients and a murine model induced by intratracheal administration of lipopolysaccharide (LPS). The key proteins involving in glycolysis were robustly elevated, including HK2, PKM2, and HIF-1α. Intriguingly, inhibition of glycolysis by 2-deoxyglucose (2-DG) pronouncedly attenuated the lung tissue pathological injury, accumulation of neutrophil, oxidative stress, expression of proinflammatory factors in the lung of ALI mice induced by LPS. The 2-DG treatment also strongly suppressed the activation of the NOD-like receptor (NLR) family and pyrin domain-containing protein 3 (NLRP3) inflammasome. Furthermore, we investigated the role of glycolysis in the inflammatory response of primary murine macrophages activated by LPS in vitro. We found that the 2-DG treatment remarkably reduced the expression of proinflammatory factors induced by LPS, including tumor necrosis factor-α messenger RNA (mRNA), pro-interleukin (IL)-1β mRNA, pro-IL-18 mRNA, NLRP3 mRNA, caspase-1 mRNA, and IL-1β protein. Altogether, these data provide a novel link between gluconic metabolism reprogramming and uncontrolled inflammatory response in ALI. This study suggests glycolytic inhibition as an effective anti-inflammatory strategy in treating ALI.
Antimicrobial resistance of Escherichia coli O26 and O111 isolates from cattle and their characteristics
The present study was to investigate antimicrobial resistance profiles of Escherichia coli O26 and O111 from cattle and to characterize the virulence genes of the resistant isolates. This paper reports the high prevalence of antimicrobial resistant E. coli O26 and O111 from cattle. Among 37 E. coli O26 and 25 E. coli O111 isolates from the fecal specimens obtained from cattle, 26 (70%) and 15 (60%) were resistant to at least one antibiotic, respectively. Forty (98%) of the 41 resistant isolates were resistant to two or more antibiotics. Among the 22 antibiotics tested in this study, ampicillin was the most common antibiotic that the isolates were resistant to, followed by tetracycline and streptomycin. None of the isolates were resistant to fluoroquinolones, such as ciprofloxacin, ofloxacin and norfloxacin, and to ceftriaxone, amikacin and imipenem. Eighteen different resistant types among the 41 isolates were observed by the cluster analysis. The most frequent antibiotic-resistance type was ampicillin-tetracycline-streptomycin-cephalothin-sulfisoxazole-ticarcillin-kanamycin-minocycline-piperacillin-chloramphenicol, which accounted for 9 (22%) of the resistant isolates. The observation of frequent and multiple resistances to antibiotics highlights the need for their careful use if their benefits are to be preserved. PCR analysis of the EHEC virulence markers showed that 25 of the resistant E. coli O26 and O111 isolates tested positive for stx2 or both stx1 and stx2. This suggests that the majority of these isolates can cause serious diseases in humans and may complicate the future therapeutic options under development.
Fractions of lipopolysaccharide from Escherichia coli O111:B4 prepared by two extraction procedures
Lipopolysaccharides have been extracted from Escherichia coli O111:B4 by phenol extraction and by a new method employing aqueous butanol. Both methods yield very similar lipopolysaccharide preparations. Gel filtration chromatography of either preparation yields two physically and chemically distinct lipopolysaccharide fractions. One fraction contains lipopolysaccharide molecules with long antigenic side chains. It acts like a highly asymmetric unit with an apparent weight of 1.5 times 10-6 and is not dissociated by detergents or deacylation. The second fraction has a short antigenic side chain and can be dissociated by sodium dodecyl sulfate and Triton X-100 into units of approximately 90,000. Some properties of the lipopolysaccharide fractions vary with the method of extraction.
Average Rating: 5 (Based on Reviews and 38 reference(s) in Google Scholar.)
GLPBIO products are for RESEARCH USE ONLY. Please make sure your review or question is research based.
Required fields are marked with *