Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2006-1-9
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
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
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0303-7207
pubmed:author
pubmed:issnType
Print
pubmed:day
21
pubmed:volume
245
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
67-76
pubmed:dateRevised
2008-11-21
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
pubmed:year
2005
pubmed:articleTitle
Retinoic acid amplifies the host immune response to LPS through increased T lymphocytes number and LPS binding protein expression.
pubmed:affiliation
Unité mixte UHP - INSERM U684, Faculté de Médecine, 9 avenue de la forêt de Haye, BP 184, Vandoeuvre-les-Nancy, Cedex, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't