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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1997-10-29
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pubmed:abstractText |
Cocaine has been shown to affect immune function through the release of corticosterone. Acute administration of both cocaine and corticosterone produces an enhancement of the T-dependent antibody response to sheep erythrocytes. The T-independent antibody response to DNP-ficoll is not enhanced under identical conditions, suggesting that the T-cell is involved as a cellular target. We examined T-helper cell cytokine production following in vivo cocaine administration and found an increase in IL-4 and IL-10; while IL-2 and IFN-gamma were unaffected. The rise in Th2 cytokines is consistent with an enhanced T-dependent antibody response, a measure of humoral immunity. Because previous results showed that the enhancement by cocaine is mediated via corticosterone, the direct effects of corticosterone on Th1/Th2 in vitro cytokine production were investigated. Th1 cytokines, IL-2 and IFN-gamma, were dose-dependently suppressed by corticosterone at physiologic concentrations. In contrast Th2 cytokines, IL-4 and IL-10, exhibited a biphasic dose response curve, whereby an enhancement was observed at low doses, followed by suppression at higher doses. In order to determine the consequences of this apparent shift towards a Th2 response on a Th1 response, we looked at the delayed-type hypersensitivity response to sheep erythrocytes. This measure of cell-mediated immunity was not significantly affected by acute cocaine, however, corticosterone administration resulted in a significant suppression. These results indicate that corticosterone can produce a shift towards a Th2 predominate response, possibly at the expense of Th1-mediated responses.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adjuvants, Immunologic,
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Inflammatory Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Cocaine,
http://linkedlifedata.com/resource/pubmed/chemical/Corticosterone,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Narcotics
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0162-3109
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
37
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
25-33
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:9285241-Adjuvants, Immunologic,
pubmed-meshheading:9285241-Animals,
pubmed-meshheading:9285241-Anti-Inflammatory Agents,
pubmed-meshheading:9285241-Antibody Formation,
pubmed-meshheading:9285241-Cocaine,
pubmed-meshheading:9285241-Corticosterone,
pubmed-meshheading:9285241-Cytokines,
pubmed-meshheading:9285241-Female,
pubmed-meshheading:9285241-Hypersensitivity, Delayed,
pubmed-meshheading:9285241-Mice,
pubmed-meshheading:9285241-Mice, Inbred Strains,
pubmed-meshheading:9285241-Narcotics,
pubmed-meshheading:9285241-Spleen,
pubmed-meshheading:9285241-Th1 Cells,
pubmed-meshheading:9285241-Th2 Cells
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pubmed:year |
1997
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pubmed:articleTitle |
Disruption of Th1/Th2 cytokine balance by cocaine is mediated by corticosterone.
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pubmed:affiliation |
Department of Pharmacology and Toxicology, Medical College of Virginia/Virginia Commonwealth University, Richmond 23298-0613, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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