Steroid hormone regulation of antiviral immunity.
Identifieur interne : 002D84 ( Main/Exploration ); précédent : 002D83; suivant : 002D85Steroid hormone regulation of antiviral immunity.
Auteurs : D A Padgett [États-Unis] ; R M Loria ; J F SheridanSource :
- Annals of the New York Academy of Sciences [ 0077-8923 ] ; 2000.
Descripteurs français
- KwdFr :
- MESH :
- immunologie : Maladies virales.
- physiologie : Immunité innée, Stéroïdes.
- Animaux, Mâle, Neuro-immunomodulation, Souris, Souris de lignée C57BL.
English descriptors
- KwdEn :
- MESH :
- chemical , physiology : Steroids.
- immunology : Virus Diseases.
- physiology : Immunity, Innate.
- Animals, Male, Mice, Mice, Inbred C57BL, Neuroimmunomodulation.
Abstract
Recent observations in both humans and animals have demonstrated that stress is immunomodulatory and can alter the pathogenesis of microbial infections to the extent that it may be adverse to health. Stress disrupts homeostasis, and the body responds through endocrine and nervous system interactions in an effort to re-establish the health of the host. However, the resulting physiologic changes associated with stress, such as the rise in serum glucocorticoids (GCs), are implicated in suppression of antiviral immunity. Therefore, it would be of significance to counterregulate stress-mediated immunosuppression during viral infection to improve immune responses and limit virus-mediated damage. The data in this study focus upon the antiglucocorticoid influence of a native steroid hormone that has been shown to augment immune function and protect animals against lethal viral infections. Androstenediol (5-androstene-3 beta,17 beta-diol, AED), a metabolite of dehydroepiandrosterone (DHEA), confers protection against lethal infection with influenza A virus. The protective activity appears to counterbalance the function of the regulatory GCs because AED prevents GC-mediated suppression of IL-1, TNF-alpha, and IL-2 secretion. Furthermore, AED inhibits GC-induced transcription of a GC-sensitive reporter gene.
DOI: 10.1111/j.1749-6632.2000.tb05459.x
PubMed: 11268423
Affiliations:
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Le document en format XML
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(physiologie)</term><term>Maladies virales (immunologie)</term><term>Mâle</term><term>Neuro-immunomodulation</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Stéroïdes (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Steroids</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Maladies virales</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Virus Diseases</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Immunité innée</term><term>Stéroïdes</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Immunity, Innate</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Neuroimmunomodulation</term></keywords><keywords scheme="MESH" 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Stress disrupts homeostasis, and the body responds through endocrine and nervous system interactions in an effort to re-establish the health of the host. However, the resulting physiologic changes associated with stress, such as the rise in serum glucocorticoids (GCs), are implicated in suppression of antiviral immunity. Therefore, it would be of significance to counterregulate stress-mediated immunosuppression during viral infection to improve immune responses and limit virus-mediated damage. The data in this study focus upon the antiglucocorticoid influence of a native steroid hormone that has been shown to augment immune function and protect animals against lethal viral infections. Androstenediol (5-androstene-3 beta,17 beta-diol, AED), a metabolite of dehydroepiandrosterone (DHEA), confers protection against lethal infection with influenza A virus. The protective activity appears to counterbalance the function of the regulatory GCs because AED prevents GC-mediated suppression of IL-1, TNF-alpha, and IL-2 secretion. Furthermore, AED inhibits GC-induced transcription of a GC-sensitive reporter gene.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country></list><tree><noCountry><name sortKey="Loria, R M" sort="Loria, R M" uniqKey="Loria R" first="R M" last="Loria">R M Loria</name><name sortKey="Sheridan, J F" sort="Sheridan, J F" uniqKey="Sheridan J" first="J F" last="Sheridan">J F Sheridan</name></noCountry><country name="États-Unis"><noRegion><name sortKey="Padgett, D A" sort="Padgett, D A" uniqKey="Padgett D" first="D A" last="Padgett">D A Padgett</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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