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)

Malnutrition is frequently observed in patients with pulmonary tuberculosis. We have already reported the nutritional disturbance in those patients by comprehensive nutritional assessment. But the mechanism of this nutritional disturbance remains unclear. We anticipated that cytokines contributed to the nutritional disturbance. To elucidate this mechanism we measured the productions of interleukin-1 (IL-1) and tumor necrosis factor (TNF) by peripheral blood monocytes, and correlated them with nutritional parameters in those patients. These cytokines had been reported to mediate metabolic alterations in inflammatory process. Subjects were 45 patients with bacteriologically confirmed pulmonary tuberculosis and their controls matched by age and sex. Adherent monocyte at 0.5 x 10(6)/ml were stimulated by lipopolysaccharide (LPS), and the culture supernatant was measured by ELISA for IL-1 and TNF. In order to assess nutritional status we measured serum albumin, transferrin, prealbumin, retinol binding protein, branched chain amino acid (BCAA)/aromatic amino acid (AAA) ratio as amino acid imbalance index, % ideal body weight (%IBW), % arm muscle circumference (% AMC) as muscle mass index, % triceps skin fold thickness (% TSF), as fat store index. The results were as follows: (1) Patients with active pulmonary tuberculosis were confirmed to be malnourished in visceral proteins, plasma amino acid, and anthropometric indices. (2) In patients with moderate or mild nutritional depletion the production of IL-1 and TNF was higher than that in healthy controls, and significantly correlated inversely with the nutritional parameters. (3) In patients with severe nutritional depletion the production of IL-1 and TNF was lower than that in healthy controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Interaction between interleukin-1 and tumor necrosis factor productions by peripheral blood monocytes and nutritional disturbance in active pulmonary tuberculosis]. 189 Jul 90

The effect of vitamin A deficiency on the mitogen response of splenic B and T lymphocytes was determined in adult vitamin A-deficient rats. Female weanling Brown Norway/Billingham-Rijswijk (BN/BiRij) and Sprague-Dawley rats were fed a semipurified, essentially vitamin A-free diet, which resulted in clinical symptoms of vitamin A deficiency and severely decreased plasma retinol contents at the age of about 17 and 41 wk for BN/BiRij and Sprague-Dawley rats, respectively. A lower B cell proliferative response after stimulation with lipopolysaccharide in combination with dextran sulfate was observed in vitamin A-deficient rats of both strains, but the T cell proliferative response after concanavalin A stimulation was unchanged. The lower B cell mitogen response was not associated with changes in the cellular composition of the spleen (as analyzed with monoclonal antibodies specific for the various subsets of T and B cells and of macrophages). We suggest that the age at which clinical symptoms of vitamin A deficiency are induced may be an important determinant for the immunological variables affected.
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PMID:Mitogen response of B cells, but not T cells, is impaired in adult vitamin A-deficient rats. 194 Dec 60

The effect of retinoic acid (RA) and retinol (ROH) on the release of tumor necrosis factor (TNF) by human peripheral blood monocytes (HPBM) was determined. HPBM were cultured for various periods of time in either 5% complete (cAB) or delipidized (DLS) AB serum. TNF release (L929 cytolytic assay) in the presence of cAB occurred during the first 3 days of in vitro culture. Delipidization of AB serum completely inhibited the lipopolysaccharide (LPS)-induced release of TNF by HPBM. Addition of RA (0.5 microM) to DLS restored LPS-induced TNF release by HPBM, and supplementation with ROH (1.0 microM) resulted in release of TNF-like activity, but only after 3 days of in vitro culture. The maintenance of TNF release by the addition of exogenous RA after 3 days of in vitro culture suggested that depletion of endogenous RA was partially responsible for loss of TNF-like activity. The levels of endogenous TNF protein and mRNA were not influenced by delipidization of serum and were found to be similar to those of HPBM cultured in the presence of AB serum. TNF protein and mRNA were undetectable in HPBM ROH-treated cell lysates, although cytolytic activity was observed in culture supernatants. These results suggest that retinoids are required for the release of cytolytic factors from HPBM and that non-TNF cytolytic factors may be released by these cells at different stages of maturation.
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PMID:Effect of retinoids on the release and gene expression of tumor necrosis factor-alpha in human peripheral blood monocytes. 223 May 95

Diseases and losses were registered in dependence on vitamin A supply with 2,035 pigs (6.5-114 kg live weight). The histologic examinations comprised various organs of 72 animals. The content of the main protein fractions as well as antibody titre after supplementing antigenes were determined in the serum of 104 animals. The feeding of a vitamin-A- and carotinefree casein-starch-respectively a Vitamin-A-free cereal-soybeanmeal-diet led to deficiency symptoms after 7-8 respectively 16-19 weeks of experiment particularly in the shape of nervous disturbances and voice affectations. Histologically a hyperplasia and a metaplasia of the epithelium of the big ducts in the salivory gland could be proved. The repletion of a part of the avitaminotic animals by means of oral (500 I.U./kg feed) and parenteral (500,000 to 1,000,000 I.U. i.m.) vitamin A administration is proof of a lack of vitamin A. Vitamin A and provitamin dosage did not influence diseases and losses with the exception of the occurrence of deficiency symptoms. The protein content of the serum as well as that of the globulin fractions alpha, beta, gamma did not change, the albumin content was lower in the groups without vitamin A (p greater than 0.05). Antibody titre against the lipopolysaccharide of salmonella dublin and human gamma globulin were diminished in piglets and fattening pigs fed vitamin A free (p less than 0.05). Taking the criterion of animal health, a vitamin A requirement higher than for growth (250 I.U./kg feed) cannot be derived.
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PMID:[Vitamin A requirements of growing swine. 3. Effect of vitamin A supply on the state of health of piglets and fattening swine]. 240 96

The in vitro effect of short-term culture as well as the effect of retinol (ROH), retinoic acid (RA), muramyl dipeptide [( Abu']MDP), lipopolysaccharide (LPS), and gamma interferon (IFN-gamma) on the induction of the purine metabolic enzymes, adenosine deaminase (ADA), purine nucleoside phosphorylase (PNP), and 5'nucleotidase (5NT) in human peripheral blood monocytes (HPBM) was examined. HPBM isolated by centrifugal elutriation were cultured for up to 96 h. Following an initial time lag of 24 h, mean ADA activity from seven separate experiments as measured in nmoles/10(6) cells/h increased from a baseline of 31.3 +/- 9.3 to 57.8 +/- 16.4 (P less than 0.005) at 72 h and to 72 +/- 21.5 (P less than .025) by 96 h. 5NT activity increased from a baseline of 2.2 +/- 0.9 to a maximum of 44 +/- 10.1 by 72 h and then declined to 29 +/- 18 (P less than 0.005) by 96 h, while no significant change in PNP activity was observed. HPBM incubated for 3 d with optimal concentrations of LPS, RA, and IFN-gamma had increases in ADA and 5NT activity ranging from three- to 10-fold compared to HPBM cultured in media alone, whereas no effect was observed with ROH and [Abu']MDP. RA, but not ROH, significantly enhanced ADA activity in a monocytic leukemia cell (THP-1) line. Addition of RA or the tumor promoter, phorbol 12-myristic 13-acetate (PMA), to HPBM or THP-1 cells resulted in significant increases in 5NT activity with opposite effects on ADA activity. These findings suggest that the biological mechanisms associated with differentiation in normal and malignant monocytes seem to be related and that the sequence and degree to which the various differentiation agents induce the enzyme elevations are also related to the mechanisms of activation/differentiation.
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PMID:Induction of adenosine deaminase and 5' nucleotidase activity in cultured human blood monocytes and monocytic leukemia (THP-1) cells by differentiating agents. 284 22

Mouse resident peritoneal macrophages, activated in vitro with murine recombinant interferon-gamma and lipopolysaccharide in the presence of sera from different sources, showed marked differences in their abilities to inhibit murine adenocarcinoma cell growth, and in induced activity of the enzyme, tissue transglutaminase. The extraction of lipids from the serum abolished its ability to induce tissue TGase activity and to inhibit cytostatic activity, but these capabilities were fully restored by readdition of all trans-retinol or all trans-retinoic acid at physiological concentrations. Addition of dansylcadaverine, a competitive inhibitor of TGase, resulted in complete recovery of macrophages from retinoid-induced suppression of cytostatic activity. These results suggest that endogenous retinoids play an important role in the regulation of macrophage-mediated cytostatic activity in a process that is independent of prostaglandin secretion but seems to involve the protein cross-linking enzyme, tissue transglutaminase.
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PMID:Suppression of macrophage cytostatic activation by serum retinoids: a possible role for transglutaminase. 288 57

A study was conducted on the activity exerted by prolonged dietary supplementation with progressive amounts of retinoids on cell-mediated immune responses and the growth of transplantable tumors in mice. A few groups of BALB/c mice received 0 (group C), 50 (group A 50), 200 (group A 200), 500 (group A 500), and 1,000 (group A 1000) IU retinol palmitate/mouse/day in drinking water for 150 days. At progressive intervals mice from each group were tested for proliferative responses to concanavalin A (Con A), Escherichia coli lipopolysaccharide, interleukin-2, and interferon-gamma release to Con A. Ten mice from each group were also challenged with the 90-100% tumor-inducing dose of 3 distinct transplantable tumors. At the end of the experiment the principal organs were histologically examined, and the accumulation of vitamin A was evaluated. In groups A 200, A 500, and A 1000, an increase in the proliferative responses and production of lymphokines as compared to those in group C occurred after 60-90 days, but vanished after 150 days. The takes of the 3 tumors were impaired when the challenges were performed on days 75 and 150. This enhancement of distinct functions of cellular reactivity and resistance to transplantable tumors showed a linear relationship with the amount of supplemental retinol palmitate for the first 60-90 days. After 150 days, however, these enhancement effects vanished or tended to decrease.
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PMID:Effect of prolonged administration of low doses of dietary retinoids on cell-mediated immunity and the growth of transplantable tumors in mice. 308 48

The interaction of dietary vitamin A and beta-carotene with lactational status on the in vitro proliferation of mitogen-induced peripheral blood lymphocytes was studied. Cows were fed (IU/cow per d) 1) 53,000 IU vitamin A, 2) 213,000 IU vitamin A, or 3) 53,000 IU vitamin A plus 400 mg beta-carotene from 6 wk before to 2 wk after dry off. Lymphocytes were incubated with retinol, retinoic acid, or beta-carotene. Concanavalin A-induced blastogenesis was inhibited by 10(-6) M retinol and 10(-8) M retinoic acid in cows fed 53,000 IU vitamin A before dry off. In contrast, 10(-7) M retinol and 10(-7) M retinoic acid stimulated Concanavalin A-induced blastogenesis for cows fed vitamin A plus beta-carotene before dry off. After dry off, retinol and retinoic acid did not affect Concanavalin A-induced blastogenesis in all treatment groups. In vitro, 10(-5) M beta-carotene inhibited Concanavalin A-induced blastogenesis before and after dry off in all treatment groups. Blastogenesis in the absence of mitogen stimulation or induced by lipopolysaccharide was inhibited by all vitamins before and after dry off in all treatment groups. These data indicate that vitamin A and beta-carotene supplementation interact with lactational status to influence the responsiveness of bovine blood lymphocytes to vitamin challenge in vitro.
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PMID:Bovine vitamin A and beta-carotene intake and lactational status. 2. Responsiveness of mitogen-stimulated peripheral blood lymphocytes to vitamin A and beta-carotene challenge in vitro. 323 Jan 92

The titers of serum antibodies to natural infection with enteric and respiratory pathogens, to a food antigen and to tetanus and diphtheria toxoid were evaluated by enzyme-linked immunosorbent assay in 1,554 Ecuadorian children younger than 5 years of age. The nutritional status of the children was assessed by anthropometry and measurement of biochemical status indicators. The children were enrolled in a representative national nutrition and health survey. Antibody titers were analyzed as a function of the nutritional status of the children. For 12 of 14 antibody concentrations tested, underweight children showed lower antibody titers than did control children. The difference was statistically significant for antibody to both T-cell-dependent antigens (tetanus toxoid, rotavirus, respiratory syncytial virus) and T-cell-independent antigens (lipopolysaccharide, polyribosyl-ribitol phosphate, capsular polysaccharide). When children with a recent episode of diarrhea were excluded, many of the differences remained significant. When these children were further classified by age, only difference in titers of antibodies to respiratory syncytial virus and tetanus toxoid remained significant. No statistically significant difference was detected between underweight and control children with respect to protective antibody levels to four bacterial antigens. Anemic children showed significantly lower antibody levels to both T-cell-dependent and T-cell-independent antigens than did control children, and a higher proportion of anemic children had diphtheria antitoxin below a conservatively defined protective antibody level. No major differences in antibody titers were seen between children with different retinol and zinc concentrations in serum.
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PMID:Effect of malnutrition in Ecuadorian children on titers of serum antibodies to various microbial antigens. 771 15

The activation of latent transforming growth factor-beta (TGF-beta) by vascular endothelial cells (ECs) is regulated by cellular plasminogen activator (PA)/plasmin, transglutaminase (TGase), and latent TGF-beta levels. Because lipopolysaccharide (LPS) has been reported to reduce EC surface plasmin levels by increasing the production of the inhibitor of PA, PA inhibitor-1 (PAI-1), we have tested whether LPS might suppress latent TGF-beta activation in ECs using two different systems, namely, bovine aortic ECs (BAECs) cocultured with smooth muscle cells (SMCs) and BAECs treated with retinol. BAECs were either cocultured with SMCs after treatment with 15 ng/ml LPS or were treated with 2 microM retinol and/or 10 ng/ml LPS, and the expression of PA, surface plasmin, TGase, and the amounts of active and latent TGF-beta secreted into the culture medium were measured. The downregulation of surface PA/plasmin levels with LPS was accompanied by a profound decline of both TGase and latent TGF-beta expression as well as the suppression of surface activation of latent TGF-beta. The effect was dependent on the concentration of LPS and on treatment time. The formation of TGF-beta did not occur in cells maintained in LPS-contaminated culture medium.
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PMID:Lipopolysaccharide inhibits activation of latent transforming growth factor-beta in bovine endothelial cells. 789 98


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