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)

The inclusion of vitamin C in the drinking water of BALB/c mice was without effect on the humoral antibody response to sheep red blood cells and bacterial lipopolysaccharide. However, there was a significantly increased cell-mediated immune response as determined by increased T-lymphocyte responses to concanavalin A. This might suggest a mechanism, along with interferon enhancement, for the possible protection by vitamin C against some viral infections.
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PMID:Vitamin C and the immune response. 30 Jun 89

Lymphocytes bear receptors for a wide variety of neurotransmitters, hormones, and other mediators that influence cellular functions in part through alterations in cyclic nucleotide metabolism. A sizable list of agents that increase cyclic AMP levels now includes adenosine (Ra), epinephrine (beta), glucocorticosteroids, histamine (H2), prostaglandins (A, E), and bacterial products (lipopolysaccharide, cholera toxin). We have found no evidence for lymphocyte cyclic AMP responses to adenosine Ri agonists or to enkephalins. Present data suggest a role for cyclic AMP in promoting the differentiation of immature lymphocytes, whereas elevated cyclic AMP levels are associated with inhibition of mature, differentiated lymphocyte functions. Opposing these effects of cyclic AMP are those of cyclic GMP and an expanding collection of compounds that increase its levels: acetylcholine (muscarinic), ascorbate, calcium ionophore, hydroperoxides of arachidonic acid, hypoxanthine derivatives, interleukin 1, serotonin, thymic hormones, and plant lectin mitogens. The biochemical pathways mediating cyclic GMP increases and mechanisms by which cyclic GMP may enhance immunological responses are being intensively studied.
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PMID:Neurotransmitters, hormones, and cyclic nucleotides in lymphocyte regulation. 285 37

Articular cartilage explants from the knees of mongrel dogs release 5-10% of their proteoglycan content spontaneously when cultured for 4 days in serum-free modified Bigger's medium. A factor synthesized and secreted by lipopolysaccharide-stimulated rabbit macrophages can stimulate this release of proteoglycan by 2 to 3-fold. The release of proteoglycan in response to macrophage factor is maximal in the presence of 1.5-50 micrograms/ml L-ascorbic acid. In the absence of ascorbate, or with high levels of ascorbate (150 micrograms/ml), the effect of the factor is diminished by 50%. D-isoascorbate, reduced glutathione, or dithiothreitol cannot substitute for L-ascorbate in producing this effect, while dehydroascorbate can.
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PMID:Ascorbic acid stimulates the resorption of canine articular cartilage induced by a factor derived from activated rabbit macrophages. 392 38

Hydrolysis of the chromogenic beta-lactam nitrocefin by periplasmic beta-lactamase in intact Pseudomonas aeruginosa cells was used to assess the influence of various compounds on the permeability of the P. aeruginosa outer membrane. In addition to the five previously described outer membrane-active compounds EDTA, polymyxin B, gentamicin, poly-L-lysine, and Tris, seven other compounds were shown to increase outer membrane permeability to nitrocefin by 14- to 63-fold. These other compounds included poly-L-ornithine, neomycin, cetyltrimethylammonium bromide, nitrilotriacetate, L-ascorbate, and acetylsalicylate. In each case, Mg2+ ions antagonized, to different extents, the enhancement of outer membrane permeability. The same compounds increased the permeability of the outer membrane to the protein lysozyme and to the hydrophobic fluorescent probe 1-N-phenylnaphthylamine, although L-ascorbate and acetylsalicylate showed only very weak enhancement of uptake in these assays. In this report, we discuss the possibility that these compounds act at a common outer membrane site at which divalent cations noncovalently cross-bridge adjacent lipopolysaccharide molecules.
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PMID:Compounds which increase the permeability of the Pseudomonas aeruginosa outer membrane. 643 88

The uptake of tritiated thymidine by isolated peripheral blood lymphocytes obtained from male guinea pigs immunized with bovine serum albumin was studied in animals maintained on various amounts of Vitamin C for 28 days. Animals were pair-fed on ascorbate-free diet and were supplemented intraperitoneally with 0, 25, or 250 mg Na-ascorbate per day. Scorbutic animals lost weight rapidly during the final 2 experimental weeks. Their daily food intake averaged only 4 g/day during the last week; thus, pair-fed ascorbate-supplemented groups were also subjected to acute nutritional stress. Lymphocytes from guinea pigs receiving 250 mg Na-ascorbate per day incorporated in vitro the highest amounts of tritiated thymidine both in the absence of nonspecific mitogen and in the presence of concanavalin A or phytohemagglutinin. Responses to lipopolysaccharide were not conclusive. Total circulating white cells counts and relative numbers of T and B lymphocytes were assessed in a second study made under identical constraints. In scorbutic animals the percentage of B lymphocytes increased and that of T lymphocytes decreased continuously over the 4-week period. The opposite effect was observed in vitamin C-supplemented animals. These studies suggest that very high doses of ascorbate support elevated mitotic activity after 4 weeks of much reduced food intake.
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PMID:The effect of variations in vitamin C intake on the cellular immune response of guinea pigs. 736 3

1. Smoking exerts an inflammatory stimulus on lung macrophages, and smokers generally have low intakes of antioxidant micronutrients. This study was performed to investigate the relationship between whole-blood tumour necrosis factor production, plasma interleukin-6 and acute-phase protein concentration and antioxidant vitamins in smokers and non-smokers. 2. Measurement of tumour necrosis factor was conducted in whole blood stimulated with endotoxin (lipopolysaccharide), and interleukin-6 concentrations were measured in the plasma of smokers and non-smokers. Enzyme and dietary antioxidant concentrations and acute-phase proteins were determined in the two groups. 3. Tumour necrosis factor production and plasma interleukin-6 concentrations were 38% (P = 0.01) and 16% (P = 0.07) greater, respectively, in smokers than in non-smokers. Plasma vitamin A and E concentrations were unaffected by smoking; however, a 21% lower plasma vitamin C (P = 0.04) concentration was observed in smokers, than in non-smokers despite a similar intake of this vitamin by the two groups. 4. Concentrations of the acute-phase proteins alpha 1-acid glycoprotein, caeruloplasmin and alpha 2-macroglobulin were increased in the plasma of smokers compared with non-smokers by 39%, 28% and 12% respectively (P < 0.01). Our studies indicate that smokers have a compromised antioxidant status and elevated concentrations of tumour necrosis factor and interleukin-6 as a consequence of smoking. 5. These observations may provide some insight into the biological mechanisms underlying the pathology associated with smoking.
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PMID:Cigarette smoking influences cytokine production and antioxidant defences. 754 May 25

We studied the effects of nutrients such as vitamin C, E, B6, niacin, and methionine on the blastogenic response of splenocytes and lipid peroxidation (LPO) in lung and liver of mice exposed to SiO2 dust. The results showed that after treatment with SiO2, the blastogenic response of splenocytes decreased significantly (p < 0.001), whereas the LPO level in lung and liver increased remarkably (lung p < 0.05; liver p < 0.001). Vitamin E, C, and niacin strongly enhanced the blastogenic response of T and B splenic lymphocytes to concanavalin-A and to lipopolysaccharide (p < 0.001). The effects of methionine and B6 were much less intense. Other supplied nutrients have been shown to inhibit LPO in lung and liver of mice exposed to SiO2 (p < 0.001).
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PMID:Effects of vitamins and methionine on blastogenic response of splenocytes and lipid peroxidation in lung and liver of mice exposed to SiO2 dust. 772 88

Influenza B virus has been aetiologically linked to Reye Syndrome (RS), but the mechanism(s) by which this pathogen could disrupt liver metabolism and produce the hepatic mitochondrial injury characteristic of the syndrome are unknown. In this study, two mechanisms by which infection of hepatocytes with influenza B virus could disrupt cellular metabolism were investigated. (1) virus-induced increase in pro-oxidant iron with subsequent iron-induced lipid peroxidation (LP) and (2) increased membrane permeability. Hep G2 cells, a well-differentiated continuous human liver cell line derived from a hepatoblastoma, were infected with allantoic-fluid derived influenza B Lee/40 virus (AFDV) at a multiplicity of infection of 10 for 24 h; productive infection was confirmed by both haemagglutination of chick erythrocytes and by plaque assay. Infection of Hep G2 cells preloaded with 59Fe-transferrin resulted in increased release of 59Fe (153 +/- 17% of controls, P < 0.03). However, the iron released did not result in increased LP (assessed by thiobarituric acid reactive substances; TBARS). To confirm that this lack of of increase in TBARS was not due to insensitivity of the cell line to pro-oxidant iron, cells were exposed to 15 microM iron ascorbate for 60 min. Production of TBARS was increased (122 +/- 4% of controls, P < 0.0003). Release of 51Cr from infected cells was also increased (128 +/- 12% of controls, P < 0.05); thus the infected cells exhibited a generalized increase in membrane permeability. However, infection did not depress mitochondrial respiration (as assessed by the formation of MTT-f3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide-formazan. To determine if the combination of viral infection and soluble products of activated macrophages would affect mitochondrial respiration, infected hepatocytes were exposed to the supernatant fluid from THP-1 cells which had previously been incubated with lipopolysaccharide at 100 ng ml-1 for 18 h. This supernate did depress the formation of MTT-f (81 +/- 5% of controls, P < 0.03). We conclude that influenza B virus does productively infect Hep G2 cells, and does increase hepatocyte membrane permeability. This effect does not impair mitochondrial respiration directly. However, infection does act in concert with soluble products of activated macrophages to depress hepatic mitochondrial respiration. Whether this interaction can be explained by virus-induced permeability changes and/or other effects of infection deserves further investigation.
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PMID:Activated THP-1 cells depress mitochondrial respiration in Hep G2 cells infected with influenza B virus. 787 29

The effect of supplementation with vitamins C and E on cytokine production of healthy adult volunteers was studied in a single-blind trial. Ten subjects in each group received daily vitamin C (1 g ascorbic acid), vitamin E (400 mg dl-alpha-tocopheryl acetate), or vitamins C and E for 28 d. Plasma concentrations of alpha-tocopherol, ascorbate, and lipid peroxides as well as the production of cytokines by peripheral blood mononuclear cells (PBMCs) were measured before, during, and at the end of the supplementation and 1 wk later. PBMCs were cultured in the presence of absence of lipopolysaccharide for 24 h. The interleukin 1 (IL-1), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) in the culture supernates were assayed by enzyme-linked immunosorbent assay methods. Production of IL-1 beta and TNF-alpha in the group supplemented with vitamins C and E was significantly higher (P < 0.05) than that of the groups given vitamin E or vitamin C alone. The enhancing effect of supplementation with a combination of vitamins E and C coincided with peak plasma alpha-tocopherol and ascorbate concentrations and the lowest plasma lipid peroxide concentrations (P < 0.05) on day 14. In addition, an in vitro experiment with PBMCs showed that vitamins E and C reduced lipopolysaccharide-induced prostaglandin E2 production and enhanced TNF-alpha production. These results indicate that combined supplementation with vitamins C and E is more immunopotentiating than supplementation with either vitamin alone in healthy adults.
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PMID:Supplementation with vitamins C and E enhances cytokine production by peripheral blood mononuclear cells in healthy adults. 917 95

Lipopolysaccharide induced apoptosis and necrosis of human umbilical venous endothelial cells in a time-dependent manner. Lipopolysaccharide (1 microgram/ml)-induced apoptosis was maximal after 18 h, whereas necrosis occurred after prolonged incubation for more than 24 h. The increase in apoptosis correlated with a reduction in Bcl-2, a potent cell death inhibitor. Furthermore, lipopolysaccharide treatment upregulated Bax, which heterodimerizes with and thereby inhibits Bcl-2. Both the antioxidant N-acetylcysteine and the combination of vitamin C and E (10 microM) completely inhibited lipopolysaccharide-induced apoptosis, whereas vitamin C or E alone was less effective. The reduction of lipopolysaccharide-induced apoptosis by vitamin C and E was paralleled by an increase in Bcl-2 and a decrease in Bax protein levels. Thus, vitamin C and E seem to interfere with the Bcl-2 family of apoptosis regulators in human umbilical venous endothelial cells.
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PMID:Vitamin C and E prevent lipopolysaccharide-induced apoptosis in human endothelial cells by modulation of Bcl-2 and Bax. 899 28


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