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)

Cysteine and cystine transport activities of resting and activated mouse spleen lymphocytes were characterized in order to examine the contributions of cysteine and cystine to intracellular glutathione contents. Following stimulation with lipopolysaccharide, the lymphocytes markedly increased their capacity to transport cysteine. The uptake of cysteine was mediated mainly by the ASC system (Na+-dependent neutral amino acid transport system especially reactive with alanine, serine, and cysteine). On the other hand, both the resting and the activated lymphocytes had extremely low cystine transport activities. Because of the instability of cysteine, the culture media usually contained cystine but not cysteine. Therefore, both the resting and the activated lymphocytes rapidly decreased their glutathione contents owing to their poor capacities to take up cystine. The effects of freshly added cysteine on the cellular glutathione contents were examined in the presence of bathocuproinedisulfonate, a nontoxic copper-specific chelator that inhibits autoxidation of cysteine. Cysteine added at 25-400 microM only partially prevented the rapid decrease of the glutathione contents in fresh resting lymphocytes. In the lipopolysaccharide-activated cells, however, cysteine enhanced the cellular glutathione contents in a dose-dependent manner. These results indicate that the enhanced activity of the ASC system increases the level of intracellular glutathione in the presence of cysteine.
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PMID:Regulation of glutathione levels in mouse spleen lymphocytes by transport of cysteine. 368 Mar 92

The in vivo mitogenic responses to lipopolysaccharide or concanavalin A by spleen cells of mice exposed to 20 ppm nitrogen dioxide (NO2) for 96 hr, were evaluated. [3H]Thymidine incorporation after addition of either mitogen, was significantly lower in spleen cells from acutely NO2-exposed mice (NO2 SC) than from control mice, although cell viability was not affected. T- and B-cell mitogenic responses were inhibited to the same extent by NO2 exposure. NO2 SC responses were protected by the thiol compounds 2-mercaptoethanol, L-cysteine, and selenomethionine. No restoration of mitogenic response was observed after treatment with reduced glutathione. Mechanisms accounting for this in vivo NO2 immune toxicity, are discussed in terms of oxidative injury.
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PMID:In vivo nitrogen dioxide exposure depresses spleen cell in vitro mitogenic responses: effects of sulfur compounds. 380 31

ICR mice were treated orally with cysteine ethylester hydrochloride (ethylcysteine, 10 and 100 mg/kg) immediately before the intraperitoneal injection of yeast particles. This agent significantly potentiated phagocytosis of yeast particles by peritoneal polymorphonuclear leukocytes in mice obtained 2 hr after the yeast injection, and the treatment with this agent (3 and 30 mg/kg, p.o.) 4 hr before the injection of yeast potentiated phagocytosis of yeast particles by mouse peritoneal leukocytes. This agent (30 mg/kg, p.o.) restored the suppression of phagocytosis of mouse leukocytes by the intraperitoneal administration of cyclophosphamide (30 mg/kg, i.p.) 24 hr before the yeast injection. This agent (10-100 mg/kg, p.o.) had no effect on the decrease of peripheral leukocyte number in irradiated mice (560 rad), but restored the suppression of phagocytosis, nitroblue tetrazolium (NBT) reduction and stimulated NBT reduction by the addition of lipopolysaccharide. Furthermore, this agent (3-30 mg/kg, p.o.) potentiated phagocytosis, NBT reduction and stimulated NBT reduction of peripheral leukocytes obtained from guinea pigs 2 and 6 hr after ethylcysteine treatment. It is suggested that ethylcysteine potentiates phagocytosis and NBT reduction of leukocytes in animals, and it restores phagocytosis and NBT reduction inhibited by the treatment with cyclophosphamide or X-ray irradiation. It may be possible that this stimulating effect of ethylcysteine could be at least in part involved in the stimulation of nonspecific resistance to infection in the compromised host.
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PMID:[Effect of cysteine ethylester hydrochloride (Cystanin) on host defense mechanisms (III): Potentiating effects on phagocytosis and nitroblue tetrazolium (NBT) reduction by leukocytes of mice and guinea pigs]. 381 54

Colicin D-CA23, obtained by sonic treatment of mitomycin C-induced cells of Escherichia coli K-12 W1485 (colD), was purified by ammonium sulfate precipitation, gel filtration on Sephadex G200, ion-exchange chromatography on diethylaminoethyl cellulose, and isoelectrofocusing. Polyacrylamide-gel electrophoresis, sedimentation velocity analysis, and antigenic analysis indicated that the preparation was homogeneous. Colicin D is composed entirely of amino acids and hence is a simple protein uncomplexed with lipid or lipopolysaccharide. It contains six residues of cysteine per molecule. The molecular weight of colicin D is approximately 92,000, as determined by sodium dodecyl sulfate-polyacrylamide-gel electrophoresis and gel filtration on Sephadex G200. Its sedimentation coefficient is 4.41S. The behavior of colicin D in solutions of sodium dodecyl sulfate and 2-mercaptoethanol indicates that it does not consist of subunits and exists as a single polypeptide chain. Its high molecular weight and presence of six cysteine residues per molecule distinguish colicin D from all colicins previously described. Although colicins D and E3 have similar modes of action, their gross molecular properties are entirely different.
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PMID:Purification and characterization of colicin D. 462 24

The receptor specificity of H-2-restricted T lymphoblasts activated against trinitrobenzene sulfonate (TNBS)-coupled spleen cells was examined using an antigen binding assay. A population of Lyt-1+,2-T lymphoblasts acquired syngeneic Ia determinants during 4 days of primary culture with hapten-coupled stimulator cells. Syngeneic Ia was not reexpressed after trypsin treatment of the T cells, but was found after incubation with soluble Ia shed from lipopolysaccharide-activated blasts. Self-Ia binding was specific in that Lyt-1+,2- but not Lyt-1-,2+ cells acquired the antigen, and in that self-Ia bound more effectively than allogeneic Ia material. To determine the relationship of self-Ia binding to the recognition of foreign antigen, the binding of trinitrophenyl (TNP)-coupled plasma membrane vesicles by TNP-specific T cells was studied. TNP-vesicle binding occurred via TNP and H-2(Ia) molecules on the vesicles in that binding was inhibited with antibodies against TNP or H-2(Ia) molecules but not non-major histocompatibility complex (e.g., Ly-6.2) molecules on the vesicles. Complete inhibition of TNP-vesicle binding by an Iak-restricted TNP-specific T-cell line occurred with soluble TNP-lysine, but not an unrelated hapten, N-iodoacetyl-N-(5-sulfonic-1-naphthyl)ethylenediamine (I-AED)-cysteine. Conversely, I-AED-cysteine, but not TNP-lysine, inhibited binding of I-AED-coupled B6 vesicles by B6 anti-I-AED T cells. Significant, but weak inhibition of TNP-vesicle binding by the anti-TNP line was observed with glycoprotein preparations containing partially purified self-Ia molecules. However, inhibition was specific for I-Ak molecules, in that inhibition was lost after removal of I-Ak molecules from the glycoprotein preparation, and very little inhibition occurred with soluble glycoproteins prepared from thymocytes which contained very little Ia material or from LPS blasts of an unrelated H-2 haplotype. These results suggest a recognition model in which TNP and Ia determinants are recognized by neighboring receptor combining sites.
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PMID:Receptor specificity of Ia-restricted T lymphoblasts activated against trinitrobenzene sulfonate-coupled spleen cells: recognition of distinct trinitrophenyl and Ia moieties. 619 19

Cysteine ethylester (10 approximately 100 mg/kg, p.o.) augmented the production of hemolytic plaque-forming cells (HPFC) to sheep red blood cells and lipopolysaccharide in the spleen of mice. It showed no effect, however, on the HPFC production to trinitrophenylated polyvinylpyrrolidone; and it had no activity as a polyclonal B cell activator like lipopolysaccharide. Cysteine ethylester at a concentration of 3 microM or more potentiated the phagocytosis of yeast by the peritoneal polymorphonuclear leukocytes of rats. This activity was less potent than that of levamisole and D-penicillamine. It also potentiated the reduction of nitroblue tetrazolium (NBT) by blood leukocytes prepared from guinea pigs and a human being. This activity was more potent than that of levamisole and D-penicillamine. Furthermore, cysteine ethylester at doses showing an immunopotentiating activity protected irradiated mice from death by spontaneous infection. These findings suggest that this drug may have a capacity to potentiate the host defense mechanisms.
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PMID:[Effect of cysteine ethylester hydrochloride (Cystanin) on host defense mechanism]. 635 29

Growth of Neisseria gonorrhoeae strain F62 on medium containing pyruvate and a high ratio of cysteine to cystine resulted in functional and structural changes that are consistent with phenotypic changes in lipopolysaccharide. Both transparent (O-) and moderately opaque (O+) variants became more sensitive to killing by normal human serum and resistant to killing by pyocin G, a bacteriocin from Pseudomonas aeruginosa. Electrophoresis of outer membranes in the presence of sodium dodecyl sulfate demonstrated differences also dependent upon the growth medium. When gels were treated with periodic acid and stained with silver, lanes containing outer membranes obtained after growth in the modified medium demonstrated two bands in addition to those independent of the growth medium. The enhancement of these additional bands by periodate treatment indicated that they represent material containing carbohydrate. The mechanism by which the changes in the growth medium affected the surface of N. gonorrhoeae is not known; however, the changes demonstrated by electrophoresis were dependent upon either the high concentration of cysteine or the high ratio of cysteine to cystine.
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PMID:Induced changes in the surface of Neisseria gonorrhoeae. 641 13

Addition of pyruvate to growth medium failed to induce the changes in Neisseria gonorrhoeae that have been reported previously. Addition of 3.8 mM sulfite or 1.3 mM sulfite plus 14 mM pyruvate restored the medium's reactivity in a test for cysteine and its ability to induce changes in N. gonorrhoeae. The induced changes that were restored were (i) increased colonial opacity and roughness, (ii) increased sensitivity to killing by normal human serum, and (iii) electrophoretic changes that may represent changes in lipopolysaccharide. Further characterization of the electrophoretic changes showed that the bands were resistant to treatment with proteinase K, that they were not affected by EDTA and urea, and that they were not dependent upon the stage of growth.
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PMID:A role for sulfite in inducing surface changes in Neisseria gonorrhoeae. 643 4

Seven thiol compounds, namely, 2-mercaptoethanol (2-ME), alpha -thioglycerol (alpha -TG), dithiothreitol (DTT), cysteamine, L-cysteine (Cys), glutathione (GSH), and sodium thioglycollate (TGL) were examined for their mitogenic activities, the effects on mitogen-induced 3H-thymidine uptake, and the effects on antibody synthesis in vitro in murine spleen lymphocytes. All these thiols showed mitogenic activities in RPMI-1640 medium containing 10% fetal calf serum (FCS) with the following order of effectiveness: 2-ME greater than or equal to alpha -TG greater than DTT greater than cysteamine greater than Cys greater than or equal to GSH greater than TGL. A close correlation was observed between the enhancement of the response to lipopolysaccharide (LPS) and the mitogenic activities of these thiol compounds in their magnitude and dose-response profiles. The primary antibody response in vitro to sheep red blood cells (SRBC) (thymus-dependent) or dinitrophenyl (DNP)-Ficoll (thymus-independent) was augmented in a similar fashion by these compounds. T-cells depletion did not influence the enhancement by 2-ME of the antibody response to DNP-Ficoll. There was a discrepancy between the dose-response profiles of mitogenic activities of these compounds and their augmenting effects on antibody responses. Particularly, 2-ME and DTT significantly enhanced the antibody response to DNP-Ficoll or SRBC even at the nonmitogenic doses. Ethyl mercaptan (HSCH2 CH3) showed similar activities to 2-ME, but methylthioethanol (CH3 SCH2 CH2 OH) and ethanol (CH3 CH2 OH) were inactive, thus indicating that the thiol group would play an essential role in the above activities of 2-ME.
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PMID:Activation of murine lymphocytes by 2-mercaptoethanol and related thiol compounds and its mechanism. I. Relationship between mitogenic activities and augmenting effects on antibody synthesis in vitro. 697 54

The mechanism of augmentation of the primary antibody response in vitro by 2-mercaptoethanol (2-ME) was investigated. By using cystine-free RPMI 1640 medium, it was demonstrated that cyst(e)ine was absolutely required for eliciting the following murine lymphocyte reactions: antibody response to sheep erythrocytes, proliferative response to concanavalin A or lipopolysaccharide (LPS), and polyclonal antibody response induced by LPS. The maximal antibody response was attained with 2.5-5 mM cysteine or half-cystine. The serial feeding of fresh cysteine markedly amplified its capacity to support antibody response particularly when cysteine concentration was suboptimal. Such an effect was not observed in the serial addition of cystine. On the other hand, the dose-response curve of cystine was dramatically shifted to lower concentrations by the addition of 2-ME (1 x 10(-5) M), which alone could not elicit the antibody response in the absence of cystine, nor could it augment furthermore the maximal response induced by 2.5 mM half-cystine. Commercially available RPMI 1640 medium contains 0.41 mM half-cystine, which proved to be a suboptimal concentration for eliciting the maximal response. 35S-cystine was incorporated into murine lymphocytes five to six times more slowly than 35S-cysteine. The rate of cystine uptake, however, was accelerated by 2.5-fold in the presence of 1 x 10(-5) M 2-ME. A close correlation was observed between dose-response profiles of 2-ME in augmenting the antibody response and the stimulation of cystine uptake. These results strongly suggest that one of the roles of 2-ME in augmenting the antibody response in vitro is to facilitate the use of cystine contained in RPMI 1640 medium only at a suboptimal concentration.
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PMID:Mechanism of augmentation of the antibody response in vitro by 2-mercaptoethanol in murine lymphocytes. I. 2-Mercaptoethanol-induced stimulation of the uptake of cystine, an essential amino acid. 704 May 90


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