| Pyruvate prevents restraint-induced immunosuppression via alterations in glucocorticoid responses. | |
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MedLine Citation:
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PMID: 15178646 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Stress-evoked immunosuppression may reflect increased demands on cellular energy signaled via elevated glucocorticoid concentrations. We hypothesized that treatment with pyruvate, an alternative energy source, would ameliorate restraint-induced elevation of glucocorticoids and that this reduction in glucocorticoid exposure will prevent stress-induced immunosuppression. We provided exogenous pyruvate to mice exposed to repeated restraint and then assessed splenocyte counts and splenocyte proliferation in response to the mitogen, concanavalin A as well as IgM production in response to keyhole limpet hemocyanin. Immune function was suppressed in mice undergoing repeated restraint but not in mice exposed to repeated restraint followed by pyruvate treatment. All mice exposed to restraint, regardless of pyruvate supplementation, displayed equivalent occurrences of repeated elevations in corticosterone concentrations; however, the cumulative exposure to corticosterone after one episode of restraint was reduced in those mice treated with pyruvate after restraint. Finally, we tested the immunoprotective ability of pyruvate supplementation in the presence of chronically elevated corticosterone. Mice implanted with restraint-like concentrations of corticosterone after adrenalectomy decreased splenocyte counts, compared with either unmanipulated mice or mice that were implanted with a cholesterol pellet after adrenalectomy, regardless of pyruvate supplementation. These data suggest that pyruvate does not possess immunoprotective properties in the presence of chronically elevated corticosterone. Pyruvate supplementation preserves immune function during exposure to repeated restraint stressors; altered dynamics of corticosterone concentrations after pyruvate administration may mediate this immunoprotection. Pyruvate prevents restraint-induced immunosuppression via alterations in the glucocorticoid response to restraint. |
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Authors:
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Gretchen N Neigh; Stephanie L Bowers; Leah M Pyter; Michelle L Gatien; Randy J Nelson |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S. Date: 2004-06-03 |
Journal Detail:
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Title: Endocrinology Volume: 145 ISSN: 0013-7227 ISO Abbreviation: Endocrinology Publication Date: 2004 Sep |
Date Detail:
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Created Date: 2004-08-23 Completed Date: 2004-09-28 Revised Date: 2008-11-21 |
Medline Journal Info:
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Nlm Unique ID: 0375040 Medline TA: Endocrinology Country: United States |
Other Details:
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Languages: eng Pagination: 4309-19 Citation Subset: AIM; IM |
Affiliation:
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Townshend Hall, 1885 Neil Avenue Mall, Columbus, Ohio 43210, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antibody Formation / immunology Body Weight Cell Count Cell Division / immunology Corticosterone / blood Corticotropin-Releasing Hormone / metabolism Glucocorticoids / immunology* Immune Tolerance / drug effects*, physiology* Insulin / blood Leptin / blood Male Mice Mice, Inbred C57BL Paraventricular Hypothalamic Nucleus / metabolism Pyruvic Acid / pharmacology* Restraint, Physical Signal Transduction / drug effects, immunology Spleen / cytology Stress, Physiological / immunology* |
| Grant Support | |
ID/Acronym/Agency:
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MH 6614/MH/NIMH NIH HHS; MH57355/MH/NIMH NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Glucocorticoids; 0/Leptin; 11061-68-0/Insulin; 127-17-3/Pyruvic Acid; 50-22-6/Corticosterone; 9015-71-8/Corticotropin-Releasing Hormone |
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