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)

1. In the study, the effect of zinc deficiency, a natural killer (NK), and lipopolysaccharide (LPS) activated NK cell activity were investigated. 2. Rats were fed with zinc-deficient and normal diet for 3 weeks. 3. NK and LPS activated NK cell activity was 7.2 +/- 1.8%/10(6) cells (n = 10) and 9.5 +/- 4.3%/10(6) cells (n = 10), respectively, in the zinc deficient group. In the control group fed with normal diet, NK and LPS activated NK cell activity was 22.2 +/- 3.3%/10(6) cells (n = 10) and 32.5 +/- 3.5%/10(6) cells (n = 10), respectively. 4. Plasma zinc concentration was 131.7 +/- 8.8 micrograms/dl in the zinc-deficient group and 206 +/- 17.7 micrograms/dl in the control group. 5. The results suggest that decreased NK and LPS activated NK cell activity is associated with zinc deficiency.
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PMID:Decreased natural killer (NK) cell activity in zinc-deficient rats. 789 66

To determine whether cytokines or lipopolysaccharide (LPS) are involved in the induction of superoxide dismutase (SOD) in the nervous system, we examined the effects of these substances on the levels of SOD in cultured mouse astrocytes. Treatment of astrocytes with 10(2) to 10(4) U/ml tumor necrosis factor-alpha for 3 days increased the levels of Mn SOD in a dose- and time-dependent manner to as much as six times the level under nontreated conditions. Treatment with 1.0 microgram/ml LPS for 3 days elicited a fourfold increase in levels of Mn SOD, and the effect of LPS was also dose dependent. Furthermore, Mn SOD in astrocytes was induced by a 3-day exposure to interleukin-1 alpha at concentrations of 10(2) or 10(3) U/ml. However, these stimuli had no effect on levels of copper-zinc SOD (Cu/Zn SOD) in astrocytes. By contrast, interferon-gamma did not change the levels of either Mn or Cu/Zn SOD in the cells. The results indicate that the selective induction of Mn SOD by cytokines and LPS, which has been observed in nonnervous tissues, may also occur in nervous tissues. The induction of Mn SOD may represent a mechanism for protection of cells from oxidative stress.
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PMID:Induction of manganese superoxide dismutase by cytokines and lipopolysaccharide in cultured mouse astrocytes. 803 84

The potential usefulness of ELISA based serological tests to assist in rapid, early and specific diagnosis of tuberculosis was investigated. The materials were selected, based on published data and on our preliminary findings. Initially screening tests were performed using crude antigens such as Purified Protein Derivate (PPD) and a BCG-filtrate. Unfortunately, the results with these antigens were not promising. The specificity of both antigens using sera from 94 healthy controls was 64%. As a consequence of these findings, the crude antigens were excluded from further tests, and the study was continued with purified antigens. The work focused on 2 purified proteins: Antigen 60 (A60), a lipopolysaccharide-protein complex, and P32, a stress protein produced in zinc deprived cultures, identified as Antigen 85 A in the BCG reference system, both isolated from Mycobacterium bovis BCG. The commercial A60 based ELISA and our own P32 based ELISA were used to test a total of 300 sera from HIV positive, negative and unscreened individuals, mainly originating from Burundi. These sera were collected from clinical established cases of pulmonary TB, extrapulmonary TB, and patients with non-tuberculous tropical diseases such as salmonellosis, trypanosomiasis, malaria, etc. and healthy individuals. The A60 based ELISA had a sensitivity of 76.8% for the proven cases of active pulmonary tuberculosis and 61.9% for the extrapulmonary tuberculosis cases. No difference was shown between HIV positive and HIV negative patients. Specificity reached 95.2% for healthy individuals, but dropped to 68.1% when persons with active non-tuberculous tropical diseases were included. Eighty-six percent of the pulmonary cases and 87.7% of the extrapulmonary cases were detected by the ELISA-P32. These findings suggest that this test might be useful as a confirmatory test for the diagnosis of extrapulmonary tuberculosis. Again no difference was noticed between HIV negative and positive patients. The main contraindication for the use of the ELISA-P32 for the diagnosis of tuberculosis is its low specificity: 70.2% with sera from healthy controls and 22.2% for hospitalised patients and persons with non-tuberculous tropical diseases. In a small recent prospective study 4 out of 10 HIV+ persons with no evidence for TB yielded a positive result for the ELISA-P32. Two of them developed pulmonary tuberculosis within 6 months, whereas 2 P32-positives and 6 P32-negatives remained up to now without any manifestations of tuberculosis. The difference was not significant, but the number of cases was limited.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Rapid, early and specific diagnosis of tuberculosis and other mycobacterial diseases in Burundi. 812 78

We have cloned a full length complementary DNA (cDNA) of the porcine tumor necrosis factor alpha (pTNF-alpha) gene and expressed it in porcine and murine cells. Total RNA obtained from lipopolysaccharide (LPS) stimulated porcine peripheral blood mononuclear cells was reverse transcribed with a specific antisense pTNF-alpha primer to generate a single stranded cDNA which was subsequently amplified by the polymerase chain reaction utilizing an additional pTNF-alpha specific sense primer. The resulting double stranded cDNA was introduced into the pBMGNeo expression vector and transfected by electroporation in porcine (PK(15)) and murine (L929) cell lines. TNF-alpha bioactivity was detected in the supernatant of the transfected cells using a standard L929 bioassay or a PK(15) bioassay. The activity was zinc inducible as expected for a gene controlled by a metallothionein promoter. The bioactivity was not lowered by an anti-mouse TNF-alpha antiserum neutralizing murine, but not human TNF-alpha and a broad immunoreactive band of 17-19 kD was detected using an anti-mouse TNF-alpha serum suitable for immunoblotting. This newly developed tool will allow us to investigate the role of TNF-alpha in pathogenesis of viral infections and gram-negative sepsis.
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PMID:Cloning and expression in mammalian cells of porcine tumor necrosis factor alpha: examination of biological properties. 825 38

The capability of human promyelocytic leukemia cells HL60 to be induced to differentiate to various stages along the monocytic or myelocytic pathway was exploited for investigation of the uptake of selected photosensitizers by diverse types of cells of the same origin. The results showed that there was no substantial difference in photofrin uptake between noninduced HL60 cells, immature monocytes, immature neutrophils and cells differentiated along the eosinophilic pathway. In contrast, HL60 cells differentiated into macrophages (HL60 phi) exhibited markedly increased photofrin uptake, which was further enhanced by their pretreatment with bacterial lipopolysaccharide. Similar results were obtained with other photosensitizers tested: di- and tetrasulfonated aluminum phthalocyanines (A1PcS2 and A1PcS4), tetrasulfonated zinc phthalocyanine (ZnPcS4), tetraphenylporphine tetrasulfonate (TPPS4) and benzoporphyrin derivative monoacid (BPD). Despite marked differences in the state of self-aggregation and other chemical properties of these compounds, the degree of their preferential uptake by HL60 phi cells showed very little variation. In a typical experiment, the uptake of these photosensitizers by HL60 phi cells was four to five times higher than the uptake by noninduced HL60 cells. In addition to the fluorometric assay employed in most of the experiments, cellular concentration of A1PcS4 was determined by measurement of elementary aluminum using atomic absorption spectroscopy.
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PMID:The effect of differentiation on photosensitizer uptake by HL60 cells. 828 22

The metal-binding protein metallothionein (MT) confers resistance to the toxic effects of metals. Although a role for MT in metal homeostasis and protection against toxic free radicals has been suggested, no clear physiological function has been established. The ability of human monocytes to be activated by bacterial lipopolysaccharide (LPS) treatment provided a model to investigate the effect of zinc on both cellular activation (H2O2 production) and MT expression. In both primary human monocytes and a monocyte-derived cell line (THP-1), LPS induced activation and MT expression; it did not induce MT expression in nonmonocyte human cells. Treatment of THP-1 cells with nontoxic zinc levels increased MT accumulation. Subsequent treatment with LPS resulted in a decrease in both MT mRNA and protein levels and inhibited the ability of THP-1 cells to undergo the respiratory burst. Pretreatment with cadmium had the same inhibitory effect. We conclude that MT expression is associated with monocyte activation, and exposure to zinc or cadmium interferes with the ability of monocytes to respond to activation signals. Metallothionein may play a role in that response.
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PMID:Activation of human monocytes with lipopolysaccharide induces metallothionein expression and is diminished by zinc. 829 Oct 64

The present study was undertaken in rats to determine whether zinc protects against endotoxin hepatotoxicity and mortality. Treatment with zinc (50-200 mumol/kg body weight) alone or endotoxin (lipopolysaccharide B, Escherichia coli 026:B6, Difco, 2 mg/kg body weight) alone did not induce significant morphological changes in the liver parenchyma or any abnormalities in liver function tests. The mortality rate was 0%. In the rats pretreated with 100 mumol of zinc and then injected with endotoxin, the mortality rate, the incidence of focal hepatocellular coagulative necrosis and serum transaminase activity increased markedly. Eleven of the 12 rats pretreated with 200 mumol of zinc died within 4 h after endotoxin injection. In the rats pretreated with 50 mumol of zinc and then injected with endotoxin, there was no conspicuous change, in the mortality rate, liver function tests or morphology of the liver. These experimental data indicate that zinc increases the mortality rate in endotoxemic rats and augments biochemical and morphological evidence of endotoxin hepatotoxicity.
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PMID:Augmentation of endotoxin hepatotoxicity by zinc. 831 22

We investigated whether or not tolerance of the febrile and metabolic responses to human recombinant interleukin-1 beta (IL-1 beta) develops in rabbits. Febrile tolerance to bacterial endotoxin was induced by daily injections of lipopolysaccharide (LPS, 5.0 micrograms/kg iv). In LPS-tolerant rabbits, the second phase of the biphasic fever induced by intravenous injections of LPS (5.0 micrograms/kg) or IL-1 beta (2.0 micrograms/kg) was significantly reduced. However, the first phase was almost the same as that observed in normal rabbits. Five daily injections of IL-1 beta (2.0 micrograms/kg iv) resulted in the development of tolerance of the febrile response to IL-1 beta. In IL-1 beta-tolerant rabbits, the second peak of the biphasic fever was significantly reduced. In addition, decreases in leukocyte count and plasma zinc induced by intravenous injections of LPS or IL-1 beta were significantly reduced in LPS- or IL-1 beta-tolerant rabbits. However the monophasic fever induced by a smaller dose of IL-1 beta (0.5 microgram/kg iv) and the first peak of the IL-1 biphasic fever were almost the same as those observed in normal rabbits. Febrile responses induced in LPS- or IL-1 beta-tolerant rabbits by intracerebroventricular injections of LPS (5.0 ng) or IL-1 beta (2.0 ng) were similar to those observed in normal rabbits. The present results suggest that tolerance of the febrile and metabolic responses to IL-1 beta is developed after repeated injections of IL-1 beta and that reduced responsiveness to IL-1 beta is partly involved in the development of LPS tolerance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Febrile and metabolic tolerance to endotoxin and human recombinant interleukin-1 beta in rabbits. 832 71

Intraperitoneal injection of lipopolysaccharide (LPS) at a dose of 50 micrograms/kg increased the activity and the mRNA level of manganese superoxide dismutase (Mn-SOD) but did not change those of copper/zinc-SOD (Cu/Zn-SOD) in the rat pancreas. Both the formation of pancreatic edema and the elevation of serum amylase during caerulein pancreatitis were significantly relieved in the rats pretreated with LPS (50 micrograms/kg) compared with the rats without the pretreatment. These results support the view that superoxides play a key role in the pathogenesis of caerulein pancreatitis, and that Mn-SOD in the pancreas may work as a defense against the development of this disease.
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PMID:Lipopolysaccharide induces manganese superoxide dismutase in the rat pancreas: its role in caerulein pancreatitis. 855 79

One mechanism by which chemicals cause cellular injury is the formation of reactive oxygen species. In vitro studies have shown that metallothionein (MT), a small metal-binding, sulfhydryl-rich, readily inducible protein, can scavenge reactive oxygen species, especially hydroxyl radicals. Nevertheless, whether or not MT protects against oxidative stress in the intact animal is not known. Experimental induction of MT could help to clarify this question, however, it is unclear whether agents that induce MT also influence known antioxidant systems. Therefore, the present study was designed to determine whether the well-known MT inducers are specific for induction of MT or whether they might also influence other hepatic systems that protect against oxidative stress. Male rats were administered cadmium chloride (Cd; 30 mumol/kg, s.c.), zinc chloride (Zn; 1000 mumol/kg, s.c.), alpha-hederin (alpha-H, 30 mumol/kg, s.c.) or lipopolysaccharide (LPS; 1 mg/kg, s.c.) 24 h prior to measurement of antioxidant systems. Zn and alpha-H increased hepatic GSH concentration 20% and 55%, respectively. Cd significantly increased, whereas LPS reduced, the activities of selenium-dependent glutathione peroxidase and glutathione reductase. Glutathione S-transferases were not altered by any of the inducers. Cd also increased DT-diaphorase activity. Cd, Zn and alpha-H all decreased catalase activity 20-35%, while the activity of superoxide dismutase was unaffected by the inducers. The amount of total cytochrome P450 enzymes and cytochrome b5 were decreased by LPS, Cd and alpha-H, while Zn appeared to have no effect. The activities of P450 enzymes towards testosterone oxidation were also decreased by LPS, Cd and alpha-H. In conclusion, all four MT inducers examined affect systems known to protect cells against oxidative stress. Therefore, using these chemicals to determine the in vivo role of MT in protecting against oxidative stress poses difficulties.
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PMID:Effect of several metallothionein inducers on oxidative stress defense mechanisms in rats. 856 Apr 99


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