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)

ZnCl2 over a very narrow concentration range was found to be mitogenic for hamster lymph node cells but not for thymocytes or splenocytes. Maximal leucine, [3H]uridine, and [3H]thymidine incorporation. Addition of 10 micron ZnCl2 was found to greatly enhance the stimulation observed with the B-lymphocyte mitogen lipopolysaccharide but not with dextran sulfate or the T-lymphocyte mitogen lipopolysaccharide but not with dextran sulfate or the T-lymphocyte mitogen concanavalin A. Although not mitogenic for splenocytes, 10 to 25 micron ZnCl2 slightly enhanced lipopolysaccharide stimulation but not concanavalin A or dextran sulfate stimulation. The effect of ZnCl2 on lipopolysaccharide stimulation was also confirmed with outbred Hartley guinea pig splenocytes and lymph node cells. Zinc chloride (50 micron) was mitogenic for both of these tissues; the response to lipopolysaccharide was enhanced by addition of 50 micron ZnCl2, but the concanavalin A response was unaffected. The possibility that the zinc effect is mediated by proteolytic mechanisms is discussed.
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PMID:Effect of zinc chloride on hamster lymphoid cells: mitogenicity and differential enhancement of lipopolysaccharide stimulation of lymphocytes. 34 10

Feeding growth mice on diets containing raw field beans (Vicia faba var. minor) as the only source of protein brought about an impairment in growth, muscle mass and liver weight. No changes in food consumption were observed, but the food intake:weight gain ratio was increased in those animals. Plasma protein, triacylglycerols and cholesterol values were not affected by the dietary treatment although serum glucose and zinc levels fell after legume intake as well as the number of circulating erythrocytes. The relative enlargement of thymus and spleen in the legume-fed mice was apparently accompanied by a reduction in the cell number and an increase in cell size, while the protein synthesis capacity followed differentiated patterns in both tissues when assessed through protein, DNA and RNA determinations. The haemagglutination titres and the number of rosette-forming cells were lower in those animals fed on the field bean diet as well as the splenic lymphocyte responses to phytohaemagglutinin, Concanavalin A or lipopolysaccharide mitogens used to evaluate the functional status of T and B lymphocytes. The present study describes, apparently for the first time in mice, the involvement of field bean intake in some immunological disturbances affecting both humoral- and cell-mediated aspects of the immune response.
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PMID:Nutritional outcome and immunocompetence in mice fed on a diet containing raw field beans (Vicia faba, var. minor) as the source of protein. 144 28

The inhibitory effect of beta-alanyl-L-histidinato zinc (AHZ) on bone resorption in tissue culture was investigated. Calvaria were removed from weanling rats (3-week-old male) and cultured for periods up to 48 h in Dulbecco's modified Eagle medium (high glucose, 4.5%) supplemented with antibiotics and bovine serum albumin. The experimental cultures contained 10(-7) to 10(-4) mol/l AHZ. The bone-resorbing factors, parathyroid hormone (1-34) (PTH; 10(-7) mol/l), prostaglandin E2 (10(-5) mol/l), interleukin-1 alpha (IL1 alpha; 50 U/ml), and lipopolysaccharide (10 micrograms/ml), caused a significant decrease in bone calcium content. The decreases in bone calcium content induced by bone-resorbing factors were completely inhibited by the coexistence of AHZ (10(-6) to 10(-4) mol/l). Also, AHZ (10(-5) mol/l) completely inhibited the PTH (10(-7) mol/l) or IL1 alpha (50 U/ml)-induced increase in medium glucose consumption and lactic acid production by bone tissue. Furthermore, AHZ (10(-5) mol/l) fairly blocked both PTH (10(-7) mol/l)-increased acid phosphatase and decreased alkaline phosphatase activities of bone tissue. The inhibitory effect of AHZ (10(-5) mol/l) on PTH (10(-7) mol/l)-stimulated bone resorption was clearly prevented by the presence of 10(-4) mol/l dipicolinate, a chelator of zinc. However, zinc sulfate (10(-7) to 10(-4) mol/l) did not inhibit the PTH (10(-7) mol/l)-stimulated bone resorption in tissue culture. These findings indicate that AHZ had a direct inhibitory effect on bone resorption in vitro, and the AHZ effect was found in the chemical form of zinc-chelated dipeptide.
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PMID:Inhibitory effect of beta-alanyl-L-histidinato zinc on bone resorption in tissue culture. 146 76

1. Paracentrotus lividus hemolysin binds erythrocytes, zymosan particles, lipopolysaccharide and laminarin surfaces but not auto and allogeneic cell membranes. 2. The binding could, at least for erythrocytes, involve phospholipids and cholesterol. 3. The protease activity of the coelomic fluid is not related to hemolysis. 4. The finding that very low concentrations of Zn2+ inactivate the hemolysin suggests a possible regulative function of the ion in the hemolytic reaction. 5. Ultrastructural observations on rabbit erythrocyte membranes indicate that most likely the transmembrane pores are induced by the lytic molecules.
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PMID:Binding properties of Paracentrotus lividus (Echinoidea) hemolysin. 167 57

In order to clarify acute-phase response in brain, we investigated induction of metallothionein (MT) genes by administrating an endotoxin (lipopolysaccharide) in rat intraperitoneum. We performed in situ hybridization on the serial brain sections to identify the cells expressing the MT genes in acute-phase. After endotoxin administration, transcripts of MT genes were detected in the arachnoideal, ependymal cells and glial cells around the Purkinje cells of the cerebellum, while no significant induction of the MT genes by zinc ion was observed in brain. These results suggest that the acute-phase response occurs specifically in at least these 3 non-neuronal cells.
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PMID:Bacterial endotoxin-induced expression of metallothionein genes in rat brain, as revealed by in situ hybridization. 171 15

CD5 expression on B cells is regulated by certain humoral factors. In a pre-B leukemia cell line 70Z/3, we found that interleukin 4 down-regulates it. Herein, we report that zinc influences spontaneous CD5 expression by this cell line as well as actions of these factors on CD5 expression considerably. In zinc-depleted culture media, spontaneous CD5 expression by 70Z/3 cells was enhanced. In contrast, the down-regulatory action of interleukin 4 was significantly reduced under culture conditions of zinc depletion. The supplementation of zinc to physiologic concentrations (1 to 2 microM) abolished such effects of zinc-depleted medium. The reduction of the suppressive action of interleukin 4 was observed at the level of gene expression. However, CD5 mRNA expression enhanced by lipopolysaccharide or NZB-SF was not further enhanced under conditions of zinc deficiency. These observations may suggest that CD5 expression by malignant or even normal B cells may be influenced by cellular/serum zinc levels.
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PMID:Zinc depletion modifies CD5 expression by 70Z/3 murine pre-B leukemia cell line. 171 63

Organ weights and the distribution of zinc and copper were compared in HLA/ICR mice that received intraperitoneal injections of 10 micrograms of Serratia marcescens lipopolysaccharide W or of sterile physiologic saline at 2 d of age. Between 5 and 28 d of age, body weight gains were similar in both groups. At 5 and 7 d of age, lipopolysaccharide W-treated mice had significantly lower thymus weights (p less than 0.01). At 7 d of age, liver weight was significantly increased (p less than 0.01) in lipopolysaccharide W-treated mice. Compared with tissue copper concentration in coeval saline-treated mice, lipopolysaccharide W treatment significantly increased copper concentration in thymus at 5 d of age (p less than 0.05) and significantly decreased concentration of this metal in liver at 7 d of age (p less than 0.05) and in spleen at 14 d of age (p less than 0.05). Liver zinc concentration was significantly lower (p less than 0.05) in 28-d-old mice that had received lipopolysaccharide W. When expressed on the basis of total organ burdens of zinc or copper, only the liver burden of zinc in 5-d-old lipopolysaccharide W-treated mice was significantly increased (p less than 0.05). Lipopolysaccharide W treatment consistently decreased copper concentration in liver cytosol and the amounts of zinc and copper bound to metallothionein, a transition metal-binding protein, in liver cytosol. These effects of lipopolysaccharide W on organ size and metal distribution may contribute to the adverse effects that persist after endotoxin exposure in early life.
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PMID:Altered organ growth and zinc and copper distribution in endotoxin-treated neonatal mice. 189 59

We are interested in potential interactions between environmental trace metal exposures and immune function. In particular, we have wondered whether dietary exposure to nickel and zinc cations can influence T and B cell proliferation and function. To study this question, we fed SJL female mice supplemental nickel and zinc sulfate from 4-8 weeks of age, and immunized the animals intraperitoneally (i.p.) with keyhole limpet hemocyanin (KLH) at 8 weeks. Eight days later, we measured antibody responses to KLH. Both IgG and IgM antibody responses to KLH were significantly depressed in vivo in the nickel fed animals (p less than 0.005). In vitro antigenic responsiveness to KLH of splenocytes from nickel fed animals was also depressed compared with control and zinc supplemented animals (p less than 0.002). This altered antigenic responsiveness persisted even after cells had been cultured for 5 days in standard media. The zinc supplemented diets did not seem to affect antibody responsiveness and proliferation. The proliferative responses of B cells to the mitogen lipopolysaccharide (LPS) were significantly depressed in Ni fed mice, but were not affected in the zinc fed animals. T cell mitogenic responses to concanavalin A were not affected in the nickel fed animals, and were enhanced in zinc fed animals. We conclude that dietary exposure to certain trace metals may induce persisting alterations in immunity in this animal model.
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PMID:The effects of exposure to dietary nickel and zinc upon humoral and cellular immunity in SJL mice. 191 29

This study investigated the relationship between zinc status and prostaglandin E2 and interleukin-1 beta production by cultured monocytes in patients with Crohn's disease. Monocyte zinc was significantly decreased in both 12 inpatients and 22 outpatients compared with controls (P less than 0.001) but lymphocyte and polymorphonuclear cell zinc were normal. When cultured monocytes from 10 outpatients with Crohn's disease were stimulated with lipopolysaccharide, prostaglandin E2 production increased markedly, coupled with a fall in monocyte zinc. In matched controls, prostaglandin E2 production was significantly less and monocyte zinc remained stable. No difference in interleukin-1 release was noted between patients and controls. The addition of prednisolone to cell cultures suppressed prostaglandin E2, interleukin-1 synthesis, and monocyte zinc did not change. Zinc chloride augmented prostaglandin E2 production in patients, but not controls, and interleukin-1 remained stable. These results demonstrate a link between low monocyte zinc concentration and excessive prostaglandin production in patients with Crohn's disease.
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PMID:Monocyte zinc and in vitro prostaglandin E2 and interleukin-1 beta production by cultured peripheral blood monocytes in patients with Crohn's disease. 202 65

Effect of zinc on an inhibitory action of cadmium to mitogen-induced lymphocyte proliferation was investigated. Cadmium at concentrations below 10 microM selectively inhibited concanavalin A-induced T-cell proliferation as compared with bacterial lipopolysaccharide-induced B-cell proliferation. Such differential susceptibility of T- and B-cell proliferation was not observed in the cases of other cations such as mercury, lead, nickel, molybdenum, chromium(VI) and arsenic (V). The inhibitory effect of 10 microM cadmium on T-cell proliferation was almost completely prevented by addition of 30 microM zinc to the culture medium, but was not by ferrous iron, nickel and copper. Further, cadmium exerted the same extent of inhibition even when it was added at 16 h after concanavalin A stimulation, and thereafter the inhibition gradually decreased. Correlated well with this observation, the protective effect of zinc was seen as far as it existed during the first 16 h of the mitogen stimulation. As intracellular cadmium content and a cadmium-induced metallothionein level were not changed by zinc addition, these observations strongly suggest that cadmium inhibits some zinc-dependent processes required for T-cell proliferation.
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PMID:Differential susceptibility of T- and B-lymphocyte proliferation to cadmium: relevance to zinc requirement in T-lymphocyte proliferation. 204 24


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