Source:http://linkedlifedata.com/resource/pubmed/id/16309824
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1-2
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pubmed:dateCreated |
2006-1-9
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pubmed:abstractText |
Vitamin A deficiency is associated with increased susceptibility to infection but the effects of Vitamin A supplementation on host response to pathogens are controversial. This study investigated the mechanisms by which all-trans retinoic acid (atRA) modulates the host immune response in an experimental model of Vitamin A supplementation before and after challenge with LPS in rats. We show here that a supplementation with five daily injections of 10mg/kg atRA increased the number of T lymphocytes in the peripheral blood. In addition, we show that atRA increased the expression of the LPS binding protein (LBP), a component of the LPS recognition system. The retinoic acid receptor (RAR)alpha agonist Ro 4060-55 but not the pan-retinoid X receptors (RXRs) agonist Ro 2573-86 mimicked the effects of atRA on LBP expression suggesting that atRA enhances LBP expression through a RARalpha-mediated pathway. In order to investigate the significance of increased LBP expression we challenged atRA-supplemented rats with the Gram-positive bacteria Listeria monocytogenes (LM) that activates the immune response independently from LBP. In sharp contrast to our previous observations that atRA supplementation enhances IFN-gamma expression and NOS2 pathway activation in LPS-challenged rats [Devaux, Y., Grosjean, S., Seguin, C., David, C., Dousset, B., Zannad, F., Meistelman, C., de Talancé, N., Mertes, P.M., Ungureanu-Longrois, D., 2000. Retinoic acid and host-pathogen interactions: effects on inducible nitric oxide synthase in vivo. Am. J. Physiol. 279, E1045-E1053], atRA did not increase the LM-induced IFN-gamma expression and NOS2 pathway activation. Overall, these data demonstrate that although atRA induces a "priming" of the immune system characterized by increased T lymphocytes number and LBP expression, the profile of the immune response depends on the inflammatory/infectious stimulus. These results could explain why Vitamin A supplementation could have beneficial/neutral or deleterious effects according to the identity of the infectious pathogen.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Acute-Phase Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Am 580,
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Bacterial,
http://linkedlifedata.com/resource/pubmed/chemical/Benzoates,
http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type II,
http://linkedlifedata.com/resource/pubmed/chemical/Nos2 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Retinoic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Tetrahydronaphthalenes,
http://linkedlifedata.com/resource/pubmed/chemical/Tretinoin,
http://linkedlifedata.com/resource/pubmed/chemical/lipopolysaccharide-binding protein
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0303-7207
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
21
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pubmed:volume |
245
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
67-76
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:16309824-Acute-Phase Proteins,
pubmed-meshheading:16309824-Animals,
pubmed-meshheading:16309824-Antibodies, Bacterial,
pubmed-meshheading:16309824-Benzoates,
pubmed-meshheading:16309824-Carrier Proteins,
pubmed-meshheading:16309824-Cell Proliferation,
pubmed-meshheading:16309824-Flow Cytometry,
pubmed-meshheading:16309824-Gene Expression Regulation,
pubmed-meshheading:16309824-Immune System,
pubmed-meshheading:16309824-Interferon-gamma,
pubmed-meshheading:16309824-Interleukin-2,
pubmed-meshheading:16309824-Lipopolysaccharides,
pubmed-meshheading:16309824-Listeria monocytogenes,
pubmed-meshheading:16309824-Liver,
pubmed-meshheading:16309824-Lymphocyte Count,
pubmed-meshheading:16309824-Male,
pubmed-meshheading:16309824-Membrane Glycoproteins,
pubmed-meshheading:16309824-Nitric Oxide Synthase Type II,
pubmed-meshheading:16309824-Rats,
pubmed-meshheading:16309824-Rats, Inbred WKY,
pubmed-meshheading:16309824-Receptors, Retinoic Acid,
pubmed-meshheading:16309824-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:16309824-T-Lymphocytes,
pubmed-meshheading:16309824-Tetrahydronaphthalenes,
pubmed-meshheading:16309824-Tretinoin
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pubmed:year |
2005
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pubmed:articleTitle |
Retinoic acid amplifies the host immune response to LPS through increased T lymphocytes number and LPS binding protein expression.
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pubmed:affiliation |
Unité mixte UHP - INSERM U684, Faculté de Médecine, 9 avenue de la forêt de Haye, BP 184, Vandoeuvre-les-Nancy, Cedex, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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