LPS-RS
| LPS-RS | Unit size | Cat. code | Docs | Price |
|---|---|---|---|---|
LPS from R. sphaeroides | 5 mg | tlrl-rslps | TDSMSDS | Please contact our distributor Add to favorite |
| LPS-RS Ultrapure | Unit size | Cat. code | Docs | Price |
|---|---|---|---|---|
Ultrapure lipopolysaccharide from R. sphaeroides | 1 mg | tlrl-prslps | TDSMSDS | Please contact our distributor Add to favorite |
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- Specifications
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LPS from R. sphaeroides
Lipopolysaccharide from the photosynthetic bacterium Rhodobacter sphaeroides (LPS-RS) is a potent antagonist of lipopolysaccharide (LPS) from pathogenic bacteria [1]. Complete competitive inhibition of LPS activity is possible at a 100-fold excess of the antagonist. LPS-RS does not induce TLR4 signaling but is detected by the LAL assay, the standard endotoxin detection assay.
InvivoGen provides LPS-RS with two grades of purity:
- LPS-RS is a standard lipopolysaccharide (LPS) preparation extracted by a phenol-water mixture. It inhibits TLR4 activity, however, as LPS-RS contains other bacterial components, such as lipoproteins, it activates TLR2.
- LPS-RS Ultrapure is extracted by successive enzymatic hydrolysis steps and purified by the previously described phenol-TEA-DOC extraction protocol [2]. This process removes contaminating lipoproteins, and therefore LPS-RS Ultrapure does not activate TLR2 while retaining the ability to inhibit TLR4 activity.
Reference:
1. Coats SR. et al., 2005. MD-2 mediates the ability of tetra-acylated and penta-acylated lipopolysaccharides to antagonize Escherichia coli lipopolysaccharide at the TLR4 signaling complex. J Immunol.;175(7):4490-8.2. Hirschfeld M. et al., 2000. Cutting edge: repurification of lipopolysaccharide eliminates signaling through both human and murine toll-like receptor 2. J Immunol. 165(2):618-22.
Back to the topSpecifications
Specificity: TLR4 antagonistLPS-RS standard is also a TLR2 agonist
Working concentration: 10 ng - 10 μg/ml
Endotoxin level: 1 x 106 EU/mg
Solubility: 5 mg/ml in water
InvivoGen provides LPS-RS with two grades of purity: Standard and Ultrapure
Back to the topContents
LPS-RS:
- 5 mg lipopolysaccharide from Rhodobacter sphaeroides (LPS-RS)
- 1.5 ml endotoxin-free water
LPS-RS Ultrapure:
- 1 mg lipopolysaccharide from Rhodobacter sphaeroides Ultrapure (LPS-RS Ultrapure)
- 1.5 ml endotoxin-free water
LPS-RS is shipped at room temperature
Upon receipt it should be stored at -20 ̊C.Upon resuspension, prepare aliquots of LPS-RS and store at 4°C for short term storage or -20 ̊C for long term storage.
Lyophilized product is stable 1 year at -20°C when properly stored.Resuspended product is stable 1 month at 4°C and 6 months at -20°C.
Avoid repeated freeze-thaw cycles.
Description
LPS from the photosynthetic bacterium Rhodobacter sphaeroides (LPS-RS) is the first potent antagonist of toxic LPS in both human and murine cells and also prevents LPS-induced shock in mice [1].
LPS-RS is penta-acylated and as other under-acylated LPS seems to utilize at least two distinct mechanisms to block LPS-dependent activation of TLR4.
The main mechanism consists of direct competition between under-acylated LPS and hexa-acylated LPS for the same binding site on MD-2, while the secondary mechanism involves the ability of under-acylated LPS:MD-2 complexes to inhibit hexa-acylated endotoxin: MD-2 complexes function at TLR4 [2-5].
Complete competitive inhibition of LPS activity is possible at a 100 fold excess of the antagonist. LPS-RS does not induce TLR4 signaling but is detected by the LAL assay, the standard endotoxin detection assay.
LPS-RS preparations (cat. code tlrl-rslps) contain lipopeptide contaminants, and therefore stimulate Toll-like receptor 2 (TLR2).
1. Qureshi, N. et al., 1999. Nontoxic RsDPLA as a potent antagonist of toxic lipopolysaccharide. p. 687-698. In: H. Brade, and S. M. Opal, and S. N. Vogel, and D. C. Morrison, eds. Endotoxin in Health and Disease 687. Marcel Dekker, New York.2. Coats SR. et al., 2005. MD-2 mediates the ability of tetra-acylated and penta-acylated lipopolysaccharides to antagonize Escherichia coli lipopolysaccharide at the TLR4 signaling complex.J Immunol.;175(7):4490-8.3. Teghanemt A. et al., 2005. Molecular basis of reduced potency of underacylated endotoxins. J Immunol. 175(7):4669-76.4. Visintin A. et al., 2005. Pharmacological inhibition of endotoxin responses is achieved by targeting the TLR4 coreceptor, MD-2. J Immunol. 175(10):6465-72.5. Saitoh S. et al., 2004. Lipid A antagonist, lipid IVa, is distinct from lipid A in interaction with Toll-like receptor 4 (TLR4)-MD-2 and ligand-induced TLR4 oligomerization. Int Immunol. 16(7):961-9.
Back to the topCitations
2020 Eur Neuropsychopharmacol. DOI: 10.1016/j.euroneuro.2019.12.121
Role of toll-like receptor 4 antagonist Lipopolysaccharide-Rhodobacter sphaeroides on acute stress-induced voluntary ethanol preference and drinking behaviour: In vivo Swiss Albino mouse model.
Chuang H.G. et al.
2020 J Neuroinflammation. DOI: 10.1186/s12974-019-1690-2
Toll-like receptor 4 agonist and antagonist lipopolysaccharides modify innate immune response in rat brain circumventricular organs.
Vargas-Caraveo A. et al.
2019 Sci Rep. DOI: 10.1038/s41598-019-54617-w
Effect of ultrapure lipopolysaccharides derived from diverse bacterial species on the modulation of platelet activation.
Vallance T.M. et al.
2019 Nat Commun. DOI: 10.1038/s41467-019-10766-0
Serum FHR1 binding to necrotic-type cells activates monocytic inflammasome and marks necrotic sites in vasculopathies.
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Specific features of human monocytes activation by monophosphoryl lipid A.
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Connections of annexin A1 and translocator protein-18 kDa on toll like receptor stimulated BV-2 cells.
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Bovine lactoferrin reduces extra-territorial facial allodynia/hyperalgesia following a trigeminal nerve injury in the rat.
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PKC-δ isoform plays a crucial role in Tat-TLR4 signalling pathway to activate NF-κB and CXCL8 production.
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2017 J Neurosci. 37(42):10154-10172.
Site-specific regulation of P2X7 receptor function in microglia gates morphine analgesic tolerance.
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Dengue virus NS1 protein activates immune cells via TLR4 but not TLR2 or TLR6.
Modhiran N. et al.
2017 FASEB J. 31(5):1891-1902.
Soluble CD14 acts as a DAMP in human macrophages: origin and involvement in inflammatory cytokine/chemokine production.
Lévêque M. et al.
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Pathogen-mimicking vaccine delivery system designed with a bioactive polymer (inulin acetate) for robust humoral and cellular immune responses.
Tummala H. et al.
2017 J Virol. JVI.00179-17.
Ebolaviruses associated with differential pathogenicity induce distinct host responses in human macrophages.
Olejnik J. et al.
2016 Exp Cell Res. S0014-4827(16)30385-8.
Lipopolysaccharide induces proliferation and osteogenic differentiation of adipose-derived mesenchymal stromal cells in vitro via TLR4 activation.
Herzmann N. et al.
2016 J Neuroimmunol. 291:29-38.
MSRV envelope protein is a potent, endogenous and pathogenic agonist of human toll-like receptor 4: Relevance of GNbAC1 in multiple sclerosis treatment.
Madeira A, Burgelin I, Perron H, Curtin 2, Lang AB, Faucard R.
2016 Mol Hum Reprod. 22(7):465-74.
Antiphospholipid antibody-induced miR-146a-3p drives trophoblast interleukin-8 secretion through activation of Toll-like receptor 8.
Gysler SM. et al.
2016 Arthritis Res Ther. 18(1):264.
Circulating exosomes from patients with systemic lupus erythematosus induce an proinflammatory immune response.
Lee JY. et al.
2015 Infect Immun. 83(1):227-38.
Bordetella pertussis naturally occurring isolates with altered lipooligosaccharide structure fail to fully mature human dendritic cells.
Brummelman J, Veerman RE, Hamstra HJ, Deuss AJ, Schuijt TJ, Sloots A, Kuipers B, van Els CA, van der Ley P, Mooi FR, Han WG, Pinelli E.
2015 Sci Transl Med. 7(304):304ra142.
Dengue virus NS1 protein activates cells via Toll-like receptor 4 and disrupts endothelial cell monolayer integrity.
Modhiran N, Watterson D, Muller DA, Panetta AK, Sester DP, Liu L, Hume DA, Stacey KJ, Young PR.
2014 J Pain. pii: S1526-5900(14)00678-6
Toll-like receptor 4 signaling contributes to paclitaxel-induced peripheral neuropathy.
Li Y, Zhang H, Zhang H, Kosturakis AK, Jawad AB, Dougherty PM
2013 J Endocrinol.216(1):61-71.
TLR4 antagonist reduces early-stage atherosclerosis in diabetic apolipoprotein E-deficient mice.
Lu Z, Zhang X, Li Y, Jin J, Huang Y.
2013 J Immunol. 191(2):922-33
Inhaled birch pollen extract induces airway hyperresponsiveness via oxidative stress but independently of pollen-intrinsic NADPH oxidase activity, or the TLR4-TRIF pathway.
Shalaby KH, Allard-Coutu A, O'Sullivan MJ, Nakada E, Qureshi ST, Day BJ, Martin JG.
2012 FEBS Lett. 586(4):319-24
Follistatin-related protein/follistatin-like 1 evokes an innate immune response via CD14 and toll-like-receptor 4.
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