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)

We have previously described an assay to quantify the serum neutralization of bacterial lipopolysaccharide which is based on a spectrophotometric Limulus amoebocyte lysate test (T.J. Novitsky, P.F. Roslansky, G.R. Siber, and H.S. Warren, J. Clin. Microbiol. 21:211-216, 1985). Studies since have shown that serum samples drawn from patients with leukemia and fever, gram-negative or gram-positive bacterial infections, or shock caused by gram-negative bacteria neutralize approximately 10-fold more lipopolysaccharide than do samples from normal controls. These findings suggested that the increased neutralization might reflect an acute-phase response and raised the question of whether it might be under the control of interleukin-1. To answer this question, we studied the neutralization of lipopolysaccharide in serum samples drawn from rabbits before and after the administration of crude interleukin-1, prepared from activated macrophage supernatants, and recombinant human interleukin-1. Crude interleukin-1 induced a 5.7-fold increase in serum neutralization 24 h after intravenous injection, and cloned interleukin-1 induced a 3.0-fold increase (P less than or equal to 0.01 and 0.05, respectively). In individual rabbits given identical doses of crude interleukin-1 on a weight basis, the serum-neutralizing ability correlated significantly with three activities of interleukin-1: rise in temperature (r2 = 0.558; P less than or equal to 0.01), decrease in serum iron (r2 = 0.534; P less than or equal to 0.01), and increase in serum copper (r2 = 0.323; P less than or equal to 0.05). We conclude that the increase in neutralization of bacterial lipopolysaccharide by serum samples drawn from patients with inflammatory states is mediated, at least in part, by interleukin-1, presumably through the induction of acute-phase serum proteins.
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PMID:Role of interleukin-1 in augmenting serum neutralization of bacterial lipopolysaccharide. 349 48

Copper(II)(3,5-diisopropylsalicylate)2 (Cu-DIPS), administered subcutaneously to mice at 80 mg/kg body weight, had marked radioprotective activity. Given 3 h before exposure to 8.0 Gy (800 rad) irradiation, Cu-DIPS increased the 42-day survival from 40% to 86%. Seven days after exposure to 8.0 Gy, there were severe reductions in spleen weight (73%) and cellularity (98%) in both Cu-DIPS- and vehicle-treated mice. Viable spleen cells collected 7 days after irradiation were totally unresponsive to mitogenic or antigenic stimulation regardless of Cu-DIPS or vehicle treatment, suggesting that Cu-DIPS did not prevent radiation-induced damage to mature lymphocytes. At 14 days, when Cu-DIPS-treated mice started to show improved survival over vehicle-treated mice, spleen weights and cellularity were 2.5- and 3.5-fold higher, respectively, in Cu-DIPS-treated mice. Treatment with Cu-DIPS not only enhanced splenic repopulation, but also accelerated the reappearance of both B and T cell reactivities. Spleen cell responsiveness to the B cell mitogen, lipopolysaccharide (LPS), and the T cell mitogen, concanavalin A (Con A), regenerated significantly faster in Cu-DIPS-treated mice. Cu-DIPS also significantly accelerated the regeneration of T-dependent antibody induction. Based on these assays of immunocompetence, Cu-DIPS-treated mice had, on average, a seven-fold greater capacity to respond to immune stimulation than vehicle-treated mice 24 days after irradiation.
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PMID:Copper(II)(3,5-diisopropylsalicylate)2 accelerates recovery of B and T cell reactivity following irradiation. 350 May 2

Metallothioneins are a family of ubiquitous, cysteine rich proteins, whose amino acidic and genomic sequences have been highly conserved during evolution. MT synthesis is induced by heavy metals, glucocorticoids and a bacterial lipopolysaccharide in vivo and in vitro. MT forms stable complexes with heavy metals. One MTIIA gene, four MTI class genes and five pseudogenes have been isolated in humans. The cluster of MT genes is located on chromosome 16. The cloned, transfected genes retain metal inducibility. The first 150 bp of the 5' flanking region of mouse and human MT genes are essential for transcription and metal regulation. Two control regions have been identified. The distal region, between -151 and -78 is essential for efficient transcription and binding of cellular factor(s) which regulates MT gene expression. In Menkes' disease, a lethal X-linked recessive disorder, copper accumulates intracellularly bound to MT. Low doses of copper induce MT synthesis in Menkes' fibroblasts, but not in normal controls. Transfection experiments using the mouse MTI promoter fused to CAT show that the effect of copper in MT transcription is in trans. Menkes' cells are more sensitive to copper than normal controls and respond to copper poisoning by synthesizing two heat-shock like proteins. A mutation affecting copper transport or metabolism is discussed.
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PMID:Metallothionein gene regulation in Menkes' disease. 353 Sep 53

The effects of intra-articular injection of small amounts of E. coli lipopolysaccharide (LPS) into the intercarpal joint of 5 ponies were studied. The LPS induced predictable changes all of which were analogous to acute bacterial infection, except that the development of signs occurred sooner after the LPS injection, and subsided within 36 hours. Fever was monophasic and peaked at 5-7 hours. The ponies exhibited depression, reduced or absent appetite, increased pulse and respiration rates, and lameness. The lameness became evident between 1 and 2 hours after injection, at which time warmth, articular effusion, and resentment to palpation of joint flexion were evident. Hematological changes included neutrophilic leucocytosis, and changes in copper, iron and zinc serum concentrations. The synovial fluid total protein, leucocyte, and alkaline phosphatase levels increased within 2 hours. The mucin precipitation, total protein and leucocyte counts in synovial fluid remained elevated long after clinical and hematological changes had subsided. The model is useful for the study of some aspects of infectious joint disease.
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PMID:An induced synovitis disease model in ponies. 355 39

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 antipyretic properties of copper (II) salicylate and its effect on plasma copper, iron, zinc and ceruloplasmin concentrations was investigated in adult rabbits at an ambient temperature of 21.5 +/- 0.5 degrees C. The experiments indicated that copper salicylate (200 mg/kg/h i.v.) was a more potent antipyretic than sodium salicylate given in the same manner and doses. This pharmacological activity was found on a model of experimental fever induced by i.v. injection of lipopolysaccharide Escherichia coli at a dose of 1 microgram/kg. Furthermore, unlike sodium salicylate, this copper complex caused a decrease in core temperature in normothermic rabbits. At the same time copper salicylate activated heat dissipation much more efficiently than the parent drug, as manifested by decreases in vasomotor tone and reversal of postpyrogen inhibition of RF. As was expected, treatment with copper salicylate increased plasma copper and ceruloplasmin levels in both normothermic and febrile rabbits. These increases did not lead to any disturbances in iron and zinc concentrations. Neither salicylate affected postpyrogen falls in plasma iron concentrations. They both, however, delayed the appearance of zinc decreases in febrile rabbits. The results of this study suggest that copper modifies the thermoregulatory effects of salicylate. Moreover, the increased amounts of this metal do not seem to disturb seriously the ionic status of the blood.
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PMID:Copper salicylate complex: thermoregulatory and biochemical effects. 383 71

Radioimmunoassays for both human copper-zinc and manganous superoxide dismutases (Cu-Zn SOD and Mn SOD, respectively) have been developed, validated, and utilized to measure the concentrations of these enzymes in cultured monocytes. Monocyte Mn SOD increased 4.7-fold over basal during 3 days of culture, an increase that was markedly enhanced by stimulation with bacterial lipopolysaccharide (LPS). Cu-Zn SOD showed a transient decrease over the culture period but was unaffected by LPS. Stimulation with muramyl dipeptide had minimal effect on Mn SOD and no effect on Cu-Zn SOD during culture, even at a concentration capable of activating the monocytes, as defined by zymosan-induced superoxide production.
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PMID:Selective induction of manganous superoxide dismutase in human monocytes. 406 26

Sheep experimentally depleted of copper (Cu) and infected with Trichostrongylus axei and Trichostrongylus colubriformis were studied for changes in white blood cell (WBC) populations, anti-parasite antibody responses and in vitro proliferative response to phytohaemagglutinin (PHA), lipopolysaccharide (LPS) and Trichostrongylus spp. antigens. Increases in circulating total WBC, lymphocyte, monocyte and neutrophil leucocyte numbers had a bimodal distribution which was related to the different developmental stages of the nematode. Eosinophil leucocyte numbers were generally lower than those of uninfected control sheep and could be associated with parasite-induced selective unresponsiveness of PHA responsive cells. The in vitro blastogenic responses of lymphocytes to PHA stimulation increased rapidly soon after infection, reaching a peak at 2 weeks, but then declined rapidly and from 5 weeks after infection responses to PHA were barely detectable. The patterns of proliferative response against LPS and Trichostrongylus spp. antigens were identical and correlated with the appearance of anti-parasite antibodies in the serum. These last three responses reached their maxima 5 weeks after infection and then stabilized at a plateau around peak levels. It was concluded that, although the changes in the host immune response could not be consistently associated with interactions between Cu deficiency and infection, the results nevertheless suggest that Cu, as a micro-nutrient, has a role in the mechanism of cell-mediated immunity in sheep infected with Trichostrongylus spp.
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PMID:Peripheral blood white cell responses during concurrent copper deficiency and gastro-intestinal nematodiasis in sheep. 406 99

The copper-albumin chelate (Cu2+-Alb), at concentrations less than 100 micrograms/ml, has potent noncytolytic antiproliferative activity for murine splenocytes stimulated by phytohemagglutinin-M, lipopolysaccharide (Escherichia coli 055:B5), or allogeneic cells and for phytohemagglutinin-M-stimulated human leukocytes. Inhibitory effects on the incorporation of [3H]leucine into trichloroacetic acid-precipitable protein is observed only at concentrations of Cu2+-Alb above 1 mg/ml. Only albumins with a histidine residue at position number 3 (rabbit, human, bovine) which bind one copper molecule at a high affinity site are capable of eliciting Cu2+-dependent suppression. Canine albumin, which has a tyrosine residue at position 3 and does not bind Cu2+, is nonsuppressive . Copper-albumin is suppressive in both the G1 and S phases of the cell cycle, thus clearly differentiating its suppressive activity from that of normal human plasma. It is not clear, however, if the Cu2+-Alb chelate is the active suppressive species or whether albumin is more efficient than other Cu2+ chelates in donating Cu2+ to another suppressive molecule. The biological significance of Cu2+-Alb-induced suppression is unknown. Although several possibilities are discussed, the potential to generate "artifactual" suppression by the formation of Cu2+-Alb chelates as a result of protein isolation procedures using Cu2+-contaminated reagents is considered to be an important potential problem.
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PMID:Suppression of lymphocyte proliferation by copper-albumin chelates. 623 4

Plant lectin-induced proliferation of lymphocytes in vitro in both whole-spleen cell and T cell-enriched cultures was markedly effected by depletion of media copper, magnesium or zinc. The T lymphocyte-oriented mitogens concanavalin A and phytohemagglutinin and the B lymphocyte-oriented mitogen lipopolysaccharide were used to study variations in [3H]thymidine incorporation in lymphocytes cultured in media deficient in one mineral element. Since the stimulatory action of these mitogens also relates to the interaction of lymphocytes with accessory cells, we looked at the phagocytic ability of accessory cells cultured in the depleted media. In addition, we determined the variations in cell surface markers for B lymphocytes (Ia), T lymphocytes (Thy 1.2, Lyt 1 and Lyt 2) and accessory cells (Ia). Media depleted of copper, magnesium or zinc did not support normal T-lymphocyte proliferation but did support normal B-lymphocyte proliferation. The phagocytic ability of magnesium-deficient and zinc-deficient accessory cells was also depressed. This was related to depressed Ia expressions in the magnesium-deficient and zinc-deficient whole-spleen cell cultures. Total T-lymphocyte numbers, as well as Lyt 1+ cell percentages, were unchanged by media depletion, whereas Lyt 2+ cell percentages were depressed in both copper-deficient and magnesium-deficient splenocyte cultures.
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PMID:Control of in vitro lymphocyte proliferation by copper, magnesium and zinc deficiency. 633


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