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)

A 2 x 4 factorial arrangement of treatments was used in a randomized complete block designed study to determine the effects of chromium level and source on growth and immune response of stressed and non-stressed 3-wk-old crossbred weanling pigs (BW was 6.35 kg). Factors included 1) immune stress or control and 2) no supplemental Cr or .2 ppm of supplemental Cr from either CrCl3, Cr-picolinate, or Cr-nicotinic acid complex. The basal diet was a corn-soybean meal-whey diet containing 1.2% lysine. Escherichia coli lipopolysaccharide (LPS) was the stress-inducing agent and was injected on d 7, 10, and 13 of the experiment. Immune challenge with LPS resulted in reduced gain (P < .05) and feed intake (P < .10). Supplementation with Cr was not effective in alleviating the depression in growth due to LPS. However, supplementation of control pigs with Cr tended to improve (P < .10) gain and feed intake. In vitro cellular immune response as measured by a lymphocyte blastogenesis assay was increased (P < .10) in pigs fed supplemental Cr from CrCl3, or Cr-picolinate. Antibody response to sheep red blood cells tended to be increased (P < .10) in pigs supplemented with Cr-nicotinic acid, but antibody response to ovalbumin was decreased (P < .05) in pigs supplemented with organic forms of Cr. At the end of the study, effects of Cr supplementation on lymphocyte proliferative response were investigated before and after ACTH administration. Injections of ACTH resulted in increased (P < .001) serum cortisol levels and increased lymphocyte proliferation. Supplementation of Cr did not affect lymphocyte blastogenic response before or after ACTH injection (P > .10). These data suggest that Cr supplementation was not beneficial during immune stress in pigs.
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PMID:Immune response and growth of stressed weanling pigs fed diets supplemented with organic or inorganic forms of chromium. 905 63

We analyzed the influence of heavy-metal ions on human umbilical vein endothelial cells (HUVEC) in comparison to proinflammatory cytokines (TNF-alpha, IL-1beta) and lipopolysaccharide (LPS). Adhesion molecule and cytokine expressions are upregulated by heavy-metal exposure. Expression of E-selectin on the cell surface was strongly induced by 1-mM concentrations of NiCl2 and CoCl2, whereas ZnCl2 and CrCl3 had no influence. Furthermore, it is shown that NiCl2 induces mRNA expression of E-selectin, intercellular adhesion molecule-1, IL-6 and IL-8 in a 1-mM concentration. The transcription factor NF-kappaB is known to be involved in the regulation of adhesion molecule expression in endothelial cells after activation by proinflammatory cytokines. We demonstrated that treatment of HUVEC with Ni2+ and Co2+ ions induces the translocation of NF-kappaB p65 and also p50 into the nucleus. NF-kappaB binding activity is enhanced under the influence of heavy metals as determined by mobility shift analysis. P65 and p50 are components of the NF-kappaB complexes as confirmed by supershift analysis. We could show that activation at the protein level is accompanied by induction of NF-kappaB p65 mRNA expression. HUVEC also express the NF-kappaB inhibitor I kappaB-alpha (MAD-3). In the early phase of activation by Ni2+ and Co2+ ions, disappearance of I kappaB-alpha in the cytoplasm accompanied p65 translocation, followed by its gradual reappearence. Because I kappaB mRNA could be upregulated by NiCl2 as well as by a mixture of cytokines, we suggest that the replenishment of the inhibitor in the cytoplasm is caused by de novo I kappaB gene expression. In addition to the enhanced DNA-binding activity of NF-kappaB, another transcription factor, AP-1, was also augmented in HUVEC stimulated by NiCl2, CoCl2 or by proinflammatory mediators and the phorbol ester PMA. Fos protein is shown to be a component of the activated AP-1 complex, as determined by supershift analysis, suggesting that it consists of Jun/Fos heterodimers.
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PMID:Heavy metal ion induction of adhesion molecules and cytokines in human endothelial cells: the role of NF-kappaB, I kappaB-alpha and AP-1. 945 94