Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A method for estimating endotoxin by radioimmunoassay was recently introduced. The present paper describes improvements in the speed and sensitivity on this endotoxin measurement. Antigen was purified from E. coli O111: B4 (B) lipopolysaccharide by centrifugation and dialysis. Purified anti-endotoxin antibody was prepared from immunized rabbit serum. A radioimmunoassay system was established with the antigen and antibody. Dextran-coated charcoal was used to separate the antibody-bound antigen from free antigen. Experimental studies were also performed on possible factors related to the antigen-antibody reaction. Accurate measurements on quantities as low as 100 pg/ml (10ng/ml in the plasma) were performed by the dextran-coated charcoal method, and the reaction time was reduced to 2 hr at 4 degrees C. This new method does not require strict sterilization or aseptic handling, and therefore is quite practical for quantitative measurements of endotoxin.
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PMID:Measurement of endotoxin. I. Fundamental studies of radioimmunoassay of endotoxin. 13 52

Lipoprotein E. coli, a B-cell mitogen, is identified as a new agent inducing the release of endogenous C-type virus from mouse spleen cells. Like lipopolysaccharide, a previously identified inducer, this compound has a synergistic effect with 5-bromo-2'-deoxyuridine. Induced virus has the characteristic density as well as morphology of C-type viruses. Budding viruses are detected on cultured BALB/c cells by electron microscopy 2 to 4 days following culturing in the presence of lipoprotein. Pokeweed mitogen, a compound mitogenic for T- and B-cells was negative when tested for virus induction, both alone and in combination with 5-bromo-2'-deoxyuridine. Dextran sulphate, another B-cell mitogen, was negative for induction as well. However, when, combined with lipopolysaccharide, it enhanced the virus release induced by this mitogen. In contrast, no additive effects were observed either by combining dextran sulphate with other virus amplifying mitogens or by combinations of mitogens which both have virus-inducing ability. This finding is discussed with respect to B-cell differentiation.
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PMID:Mitogen induction of murine C-type viruses. IV. Effects of lipoprotein E. coli, pokeweed mitogen and dextran sulphate. 20 33

Dextran sulphate delays the onset, or even completely suppresses the expression in mice of DTH or SRBC when administered via a route different from that of eliciting antigen. However, DS injected together with the eliciting antigen potential the expression of DTH. Dextran showed no effect on DTH. Cell transfer experiments suggest that the targets for the action of DS are the accessory cells (monocytes) and not the T-effector cells. As shown, using polystyrene latex particles and lipopolysaccharide from E. coli, trapping and perhaps activation of the trapped accessory cells rather than toxic effects of DS are responsible for these phenomena.
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PMID:Suppression and potentiation of expression of delayed-type hypersensitivity by dextran sulphate. 60 84

An attempt was made to separate the antigenic and mitogenic properties of E. coli bacteria and bacterial lipopolysaccharide antigen inhibited the mitogenic response by the cultures but did not inhibit the induction of anti-LPS antibody or polyclonal antibody synthesis to SRBC. Dextran sulphate, acting as a B-cell mitogen, increased the mitogenic response in spleen cell cultures incubated with bacteria, but did not affect the production of anti-LPS antibody. Mild alkaline hydrolysis (0-1 N NaOH at 56 degrees) of LPS destroyed the mitogenic properties of the molecule, leaving the antigenic properties qualitatively intact. Harsher conditions of base hydrolysis destroyed both the mitogenic and antigenic properties of LPS, as determined by antigenicity in murine spleen cell cultures and haemagglutination inhibition tests.
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PMID:Separation of the mitogenic and antigenic responses to bacterial lipopolysaccharide. 77 Mar 15

Dextran sulphate, polyvinyl sulphate and carrageenan (but not the other polyanions tested, such as poly I:poly C, poly-L-glutamic acid or E. coli lipopolysaccharide) act synergisticaly with PHA on mouse thymocyte stimulation, as measured by thymidine uptake and blast cell transformation. Furthermore the active compounds shift the dose response of thymocytes to Con A. The effect could be observed in four different strains of mice tested by using normal or cortisone-resistant thymocytes. Two possibilities are envisaged for explanation of these effects: (a) attachment of polyanions by their anionic groups to cell surface constituents and interaction of the sulphate groups of the polymers with plant lectins; and (b) modification of the cell membrane induced by sulphated polymers changing either the binding capacity or the effectiveness of the membrane-associated events leading to thymocyte stimulation by the lectins.
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PMID:Changes in thymocyte reactivity to lectins induced by B-cell mitogens of the type of sulphated polyanions. 108 28

Dextran sulphate (DS) 500 (M.W. 500,000) is commonly used as a reticuloendothelial (RE) blocker. We found that lipopolysaccharide (LPS)-induced tumour necrosis factor (TNF) production in sera was enhanced when mice were pretreated with DS500. When mice were pretreated with DS1000 (M.W. 1,000,000), TNF activity in sera was also significantly enhanced by the LPS injection in comparison with the saline-treated group, but not by the pretreatment with the low molecular weight of DS5 (M.W. 5,000), neutral dextran (Dex) 500, or positively-charged diethylaminoethyl dextran (DEAE-Dex) 500. The enhancement of LPS-induced TNF production occurred from 2 h after DS500 pretreatment. Pretreatment with DS500 or DS1000 significantly suppressed the carbon clearance from the blood in mice from 2 h after DS injection, but this suppression was not detected by the pretreatment with DS5, Dex500, or DEAE-Dex500. We suggest that negative-charge and high molecular weight are essential for dextran derivatives to enhance LPS-induced TNF production, and that the enhancing effect of DS is closely related to the suppression of the RE function.
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PMID:Priming effect of dextran sulphates on lipopolysaccharide-induced tumour necrosis factor production in mice. 157 93

The only strains of mice which are able to synthesize lambda 1-bearing antibodies in response to alpha (1-3) Dextran are those expressing the Igha allotypic haplotype or those having an Igh V region identical to Igha mice. The experiments reported here were designed to investigate whether the nonresponsiveness of mice which do not express the Igha haplotype is a consequence of an absence of a polyclonal B cell receptor for the alpha (1-3) Dextran TI-antigen. B cells of several mouse strains were stimulated with polyclonal B cell activators (PBA) known to either stimulate non-overlapping B cell subsets or to stimulate B cells at different stages of maturation, i.e., lipopolysaccharide, Nocardia delipidated cell mitogens and alloreactive T helper cells. Whereas all three PBA induced B cells from Igha mice to secrete lambda 1-bearing anti-alpha (1-3) antibodies, the PBA were incapable of inducing B cells from non-Igha mice to mount an anti-alpha (1-3) Dextran response. The data suggest that non-Igha mice lack a functional VH Dex gene for the lambda 1-bearing anti-alpha (1-3) Dextran response.
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PMID:Igh restriction of the anti-alpha (1-3) dextran response: polyclonal B cell activators induce the synthesis of anti-alpha (1-3) dextran antibodies in lymphocytes from Igha mice only. 240 43

The attachment of Pseudomonas fluorescens and an Acinetobacter sp. to hydrogel and polystyrene surfaces was investigated to evaluate the influence of adsorbed water and macromolecules on adhesion. With both organisms, there was a decrease in attachment numbers with increasing water content of the hydrogels. There was also a decrease in attachment with a decrease in water contact angle on untreated, tissue culture and sulfonated polystyrene surfaces; however, the attachment numbers were higher than would be expected on the basis of the hydrogel data. With P. fluorescens, attachment to untreated and tissue culture polystyrene was inhibited by bovine serum albumin, Escherichia coli lipopolysaccharide, and the supernatant from spent medium, both when the conditioning substances were added to the suspension of attaching cells and when they were preadsorbed onto the surfaces. Dextran inhibited attachment only when added to the bacterial suspension. Supernatants from centrifuged natural freshwater samples had no effect. Thus, hydration of a surface and the adsorption of macromolecules can reduce bacterial attachment; however, additional factors relating to the chemical composition of the substratum and polymeric stabilization of suspended cells can affect the adhesion interaction and resultant numbers of attached cells.
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PMID:Influence of substratum hydration and adsorbed macromolecules on bacterial attachment to surfaces. 242 37

We have studied lipopolysaccharide (LPS)-induced proliferation in the rat and have found that the addition of the compound Dextran sulfate (DxS), which itself is not mitogenic, to LPS stimulated cultures results in significant enhancement of cell division. A "DxS-free" supernatant from DxS stimulated spleen cell cultures is able to substitute for DxS in stimulatory activity. This supernatant possesses interleukin 1 (IL-1) activity, however, the addition of purified recombinant IL-1 to LPS-stimulated cultures does not result in augmentation of proliferation. A DxS-free supernatant from DxS stimulated adherent cells is also able to substitute for DxS in stimulatory activity. The active molecule(s) present in the adherent cell-derived DxS-free culture supernatant appears to be distinct from classical IL-1.
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PMID:Role of adherent cells in dextran sulfate-mediated enhancement of mitogen-induced B-cell proliferation. 242 4

The cellular component of an acute ocular inflammation in rabbits was measured with autologous leukocytes exogenously labeled with 111Indium tropolonate. Inflammation was induced by intravitreal bacterial lipopolysaccharide (LPS). After 16 hr blood was removed, leukocytes separated, labeled with 111Indium tropolonate and reinjected. Three cell fractions were examined: a leukocyte rich fraction which had been prepared with Dextran; and polymorphonuclear and mononuclear leukocyte fractions which had been prepared using a discontinuous Percoll gradient. Two hours after labeled leukocytes were injected, measurements of 111Indium were made in blood, plasma, the whole eye and in ocular compartments. From these data the numbers of each leukocyte population present were estimated and compared directly to histopathologic changes. Both polymorphonuclear and mononuclear leukocytes entered ocular tissues during the 2 hr period beginning 20 hr after LPS injection. Altered ocular vascular permeability was successfully measured with 125Iodine-albumin in some of these same rabbits. Both the number and type of inflammatory cell entering ocular tissues during a set period of time of the inflammatory response could thus be measured. This technique provides an opportunity to define the relationship of leukocyte infiltration and altered ocular vascular permeability in ocular tissues during the inflammatory response.
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PMID:Quantitation of acute experimental ocular inflammation with 111indium-leukocytes. 325 51


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