Neuroendocrine regulation of cytokine production during experimental influenza viral infection: effects of restraint stress-induced elevation in endogenous corticosterone.
Identifieur interne : 000A56 ( PubMed/Corpus ); précédent : 000A55; suivant : 000A57Neuroendocrine regulation of cytokine production during experimental influenza viral infection: effects of restraint stress-induced elevation in endogenous corticosterone.
Auteurs : C M Dobbs ; N. Feng ; F M Beck ; J F SheridanSource :
- Journal of immunology (Baltimore, Md. : 1950) [ 0022-1767 ] ; 1996.
English descriptors
- KwdEn :
- Adrenal Cortex Hormones (physiology), Animals, Cytokines (biosynthesis), Cytokines (drug effects), Influenza A virus (immunology), Lymphatic Diseases (immunology), Lymphocyte Count, Male, Mice, Mice, Inbred C57BL, Mifepristone (pharmacology), Neurosecretory Systems (immunology), Orthomyxoviridae Infections (immunology), Orthomyxoviridae Infections (metabolism), Orthomyxoviridae Infections (virology), Restraint, Physical, Spleen (pathology), Stem Cells, Stress, Physiological (immunology), Th1 Cells (metabolism), Th1 Cells (virology), Th2 Cells (metabolism), Th2 Cells (virology).
- MESH :
- chemical , biosynthesis : Cytokines.
- chemical , drug effects : Cytokines.
- chemical , pharmacology : Mifepristone.
- chemical , physiology : Adrenal Cortex Hormones.
- immunology : Influenza A virus, Lymphatic Diseases, Neurosecretory Systems, Orthomyxoviridae Infections, Stress, Physiological.
- metabolism : Orthomyxoviridae Infections, Th1 Cells, Th2 Cells.
- pathology : Spleen.
- virology : Orthomyxoviridae Infections, Th1 Cells, Th2 Cells.
- Animals, Lymphocyte Count, Male, Mice, Mice, Inbred C57BL, Restraint, Physical, Stem Cells.
Abstract
A murine model of influenza viral infection was used to examine the neuroendocrine regulation of cytokine production. Restraint stress (RST) was used to activate the hypothalamic-pituitary-adrenal axis and elevate corticosterone (CORT) levels in influenza A/Puerto Rico/8/34 (PR8) virus-infected C57BL/6 mice. The type II glucocorticoid receptor antagonist RU486 was used to specifically examine the modulation of PR8 virus-specific cytokine responses by CORT. RST suppressed the PR8 virus- specific production of Th1-type (IL-2 and IFN-gamma) and Th2-type IL-10) cytokines by cells from the regional lymph nodes and spleens. In addition, IL-6 production by splenocytes was inhibited by RST; however, IL-6 production by cells from the regional lymph nodes was enhanced. Treatment of mice with RU486 prevented the effects of RST, suggesting that the RST-induced alterations in cytokine responses were mediated by CORT. Furthermore, CORT was shown to inhibit the PR8 virus-specific production of both Thl-type and Th2-type cytokines in vitro at doses corresponding to the physiologic range of free plasma CORT following hypothalamic-pituitary-adrenal axis activation.
PubMed: 8757304
Links to Exploration step
pubmed:8757304Le document en format XML
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<author><name sortKey="Dobbs, C M" sort="Dobbs, C M" uniqKey="Dobbs C" first="C M" last="Dobbs">C M Dobbs</name>
<affiliation><nlm:affiliation>Department of Medical Microbiology and Immunology, College of Medicine, Ohio State University, Columbus 43210, USA.</nlm:affiliation>
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<author><name sortKey="Feng, N" sort="Feng, N" uniqKey="Feng N" first="N" last="Feng">N. Feng</name>
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<author><name sortKey="Beck, F M" sort="Beck, F M" uniqKey="Beck F" first="F M" last="Beck">F M Beck</name>
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<author><name sortKey="Sheridan, J F" sort="Sheridan, J F" uniqKey="Sheridan J" first="J F" last="Sheridan">J F Sheridan</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Neuroendocrine regulation of cytokine production during experimental influenza viral infection: effects of restraint stress-induced elevation in endogenous corticosterone.</title>
<author><name sortKey="Dobbs, C M" sort="Dobbs, C M" uniqKey="Dobbs C" first="C M" last="Dobbs">C M Dobbs</name>
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<author><name sortKey="Beck, F M" sort="Beck, F M" uniqKey="Beck F" first="F M" last="Beck">F M Beck</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adrenal Cortex Hormones (physiology)</term>
<term>Animals</term>
<term>Cytokines (biosynthesis)</term>
<term>Cytokines (drug effects)</term>
<term>Influenza A virus (immunology)</term>
<term>Lymphatic Diseases (immunology)</term>
<term>Lymphocyte Count</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mifepristone (pharmacology)</term>
<term>Neurosecretory Systems (immunology)</term>
<term>Orthomyxoviridae Infections (immunology)</term>
<term>Orthomyxoviridae Infections (metabolism)</term>
<term>Orthomyxoviridae Infections (virology)</term>
<term>Restraint, Physical</term>
<term>Spleen (pathology)</term>
<term>Stem Cells</term>
<term>Stress, Physiological (immunology)</term>
<term>Th1 Cells (metabolism)</term>
<term>Th1 Cells (virology)</term>
<term>Th2 Cells (metabolism)</term>
<term>Th2 Cells (virology)</term>
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<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Cytokines</term>
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<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Mifepristone</term>
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<keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Adrenal Cortex Hormones</term>
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<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Influenza A virus</term>
<term>Lymphatic Diseases</term>
<term>Neurosecretory Systems</term>
<term>Orthomyxoviridae Infections</term>
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<term>Th1 Cells</term>
<term>Th2 Cells</term>
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<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Spleen</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Orthomyxoviridae Infections</term>
<term>Th1 Cells</term>
<term>Th2 Cells</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Lymphocyte Count</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Restraint, Physical</term>
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<front><div type="abstract" xml:lang="en">A murine model of influenza viral infection was used to examine the neuroendocrine regulation of cytokine production. Restraint stress (RST) was used to activate the hypothalamic-pituitary-adrenal axis and elevate corticosterone (CORT) levels in influenza A/Puerto Rico/8/34 (PR8) virus-infected C57BL/6 mice. The type II glucocorticoid receptor antagonist RU486 was used to specifically examine the modulation of PR8 virus-specific cytokine responses by CORT. RST suppressed the PR8 virus- specific production of Th1-type (IL-2 and IFN-gamma) and Th2-type IL-10) cytokines by cells from the regional lymph nodes and spleens. In addition, IL-6 production by splenocytes was inhibited by RST; however, IL-6 production by cells from the regional lymph nodes was enhanced. Treatment of mice with RU486 prevented the effects of RST, suggesting that the RST-induced alterations in cytokine responses were mediated by CORT. Furthermore, CORT was shown to inhibit the PR8 virus-specific production of both Thl-type and Th2-type cytokines in vitro at doses corresponding to the physiologic range of free plasma CORT following hypothalamic-pituitary-adrenal axis activation.</div>
</front>
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<Title>Journal of immunology (Baltimore, Md. : 1950)</Title>
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<ArticleTitle>Neuroendocrine regulation of cytokine production during experimental influenza viral infection: effects of restraint stress-induced elevation in endogenous corticosterone.</ArticleTitle>
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<Abstract><AbstractText>A murine model of influenza viral infection was used to examine the neuroendocrine regulation of cytokine production. Restraint stress (RST) was used to activate the hypothalamic-pituitary-adrenal axis and elevate corticosterone (CORT) levels in influenza A/Puerto Rico/8/34 (PR8) virus-infected C57BL/6 mice. The type II glucocorticoid receptor antagonist RU486 was used to specifically examine the modulation of PR8 virus-specific cytokine responses by CORT. RST suppressed the PR8 virus- specific production of Th1-type (IL-2 and IFN-gamma) and Th2-type IL-10) cytokines by cells from the regional lymph nodes and spleens. In addition, IL-6 production by splenocytes was inhibited by RST; however, IL-6 production by cells from the regional lymph nodes was enhanced. Treatment of mice with RU486 prevented the effects of RST, suggesting that the RST-induced alterations in cytokine responses were mediated by CORT. Furthermore, CORT was shown to inhibit the PR8 virus-specific production of both Thl-type and Th2-type cytokines in vitro at doses corresponding to the physiologic range of free plasma CORT following hypothalamic-pituitary-adrenal axis activation.</AbstractText>
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