Source:http://linkedlifedata.com/resource/pubmed/id/10092810
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
1999-4-13
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pubmed:abstractText |
Certain cytokines activate the hypothalamic-pituitary-adrenal axis for glucocorticoid release, and these hormones can protect against cytokine-mediated pathologies. However, endogenous activation of such a pathway has not been established during infections. A prominent glucocorticoid response peaks 36 h following murine CMV (MCMV) infection, coincident with circulating levels of the cytokines IL-12, IFN-gamma, TNF, and IL-6, and dependent on IL-6 for maximal release. These studies examined functions of the hormone induction. Mice rendered glucocorticoid deficient by adrenalectomy were more susceptible than intact mice to MCMV-induced lethality, and the increased sensitivity was reversed by hormone replacement. Lack of endogenous glucocorticoids resulted in increases in IL-12, IFN-gamma, TNF, and IL-6 production, as well as in mRNA expression for a wider range of cytokines, also including IL-1 alpha and IL-1 beta. Viral burdens did not increase, and actually decreased, in the livers of glucocorticoid-deficient mice. TNF, but not IFN-gamma, was required for increased lethality in the absence of endogenous hormone. These results conclusively demonstrate the importance of induced endogenous glucocorticoids in protection against life-threatening effects resulting from infection-elicited cytokine responses. Taken together with the dependence on induced IL-6, they document existence of an immune system-hypothalamic-pituitary-adrenal axis pathway for regulating endogenous responses to viral infections.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
162
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3527-33
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:10092810-Administration, Oral,
pubmed-meshheading:10092810-Adrenalectomy,
pubmed-meshheading:10092810-Animals,
pubmed-meshheading:10092810-Corticosterone,
pubmed-meshheading:10092810-Cytokines,
pubmed-meshheading:10092810-Glucocorticoids,
pubmed-meshheading:10092810-Herpesviridae Infections,
pubmed-meshheading:10092810-Male,
pubmed-meshheading:10092810-Mice,
pubmed-meshheading:10092810-Mice, Inbred C57BL,
pubmed-meshheading:10092810-Mice, Knockout,
pubmed-meshheading:10092810-Muromegalovirus,
pubmed-meshheading:10092810-Survival Analysis
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pubmed:year |
1999
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pubmed:articleTitle |
Endogenous glucocorticoids protect against cytokine-mediated lethality during viral infection.
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pubmed:affiliation |
Department of Molecular Microbiology and Medicine, Brown University, Providence, RI 02912, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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