Antiglucocorticoid function of androstenetriol.
Identifieur interne : 000235 ( Ncbi/Curation ); précédent : 000234; suivant : 000236Antiglucocorticoid function of androstenetriol.
Auteurs : R M Loria [États-Unis]Source :
- Psychoneuroendocrinology [ 0306-4530 ] ; 1997.
Descripteurs français
- KwdFr :
- Adjuvants immunologiques (pharmacologie), Androstènediols (pharmacologie), Androsténols (pharmacologie), Animaux, Concanavaline A (métabolisme), Déhydroépiandrostérone (pharmacologie), Glucocorticoïdes (antagonistes et inhibiteurs), Glucocorticoïdes (pharmacologie), Interleukine-2 (biosynthèse), Interleukine-3 (biosynthèse), Lipopolysaccharides (pharmacologie), Mitogènes (pharmacologie), Rate (), Rate (cytologie), Rate (métabolisme), Souris, Souris de lignée C57BL, Thymidine (métabolisme).
- MESH :
- antagonistes et inhibiteurs : Glucocorticoïdes.
- biosynthèse : Interleukine-2, Interleukine-3.
- cytologie : Rate.
- métabolisme : Concanavaline A, Rate, Thymidine.
- pharmacologie : Adjuvants immunologiques, Androstènediols, Androsténols, Déhydroépiandrostérone, Glucocorticoïdes, Lipopolysaccharides, Mitogènes.
- Animaux, Rate, Souris, Souris de lignée C57BL.
English descriptors
- KwdEn :
- Adjuvants, Immunologic (pharmacology), Androstenediols (pharmacology), Androstenols (pharmacology), Animals, Concanavalin A (metabolism), Dehydroepiandrosterone (pharmacology), Glucocorticoids (antagonists & inhibitors), Glucocorticoids (pharmacology), Interleukin-2 (biosynthesis), Interleukin-3 (biosynthesis), Lipopolysaccharides (pharmacology), Mice, Mice, Inbred C57BL, Mitogens (pharmacology), Spleen (cytology), Spleen (drug effects), Spleen (metabolism), Thymidine (metabolism).
- MESH :
- chemical , antagonists & inhibitors : Glucocorticoids.
- chemical , biosynthesis : Interleukin-2, Interleukin-3.
- chemical , metabolism : Concanavalin A, Thymidine.
- chemical , pharmacology : Adjuvants, Immunologic, Androstenediols, Androstenols, Dehydroepiandrosterone, Glucocorticoids, Lipopolysaccharides, Mitogens.
- cytology : Spleen.
- drug effects : Spleen.
- metabolism : Spleen.
- Animals, Mice, Mice, Inbred C57BL.
Abstract
The anti-inflammatory and immunosuppressive functions of corticosteroids have been well established and characterized. In contrast, a different group of native steroids, which include dehydroepiandrosterone (DHEA) and two of its metabolites, androstenediol (5-androstene-3 beta-17 beta-diol, AED) and androstenetriol (5-androstene-3 beta-7 beta-17 beta-triol, beta AET), function in vivo to up-regulate host immune response against infections and counteract stress-induced immunosuppression. Indeed, DHEA and particularly, AED and beta AET, have been shown to protect mice from viral, bacterial, and parasitic infections. In vivo, these three hormones are in opposition to the widely demonstrated immunosuppressive action of glucocorticoids, suggesting a possible new immune regulation mechanism. The individual activity in vitro of each of these steroids, i.e. DHEA, AED, and beta AET, on a mitogen-induced mixed splenocyte proliferation assay were determined. The results showed that DHEA suppressed the proliferation of cultures activated with concanavalin A (ConA) or lipopolysaccharide (LPS) in a dose-dependent manner. AED had little influence on the activation response. However, beta AET potentiated the response to both mitogens significantly above control. The regulation of the cytokine secretion, of both interleukin-2 (IL-2) and interleukin-3 (IL-3), from ConA-activated lymphocytes was affected in the same manner. These functions were depressed by DHEA, unaffected by AED, and potently increased by beta AET. Moreover, the classic immunosuppressive effects of hydrocortisone on ConA-induced lymphocyte proliferation, as well as on IL-2 and IL-3 production, were unaffected by being co-cultured with DHEA and only minimally counteracted by AED at high doses. In contrast, co-culturing with beta AET significantly counteracted the immunosuppressive effects of hydrocortisone on lymphocyte proliferation and cytokine production. These data show that in-vivo, DHEA, AED, and beta AET may have some similar functions, while in vitro, their effects are dramatically different from one another. Only beta AET could markedly potentiate the cellular response by increasing lymphocyte activation and counteracting the immnosuppressive activity of hydrocortisone on lymphocyte proliferation and cytokine production.
PubMed: 9264155
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pubmed:9264155Le document en format XML
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<author><name sortKey="Loria, R M" sort="Loria, R M" uniqKey="Loria R" first="R M" last="Loria">R M Loria</name>
<affiliation wicri:level="1"><nlm:affiliation>Virginia Commonwealth University, Medical College of Virginia, Richmond 23298-0678, USA. Loria@gems.vcu.edu</nlm:affiliation>
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<series><title level="j">Psychoneuroendocrinology</title>
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<imprint><date when="1997" type="published">1997</date>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adjuvants, Immunologic (pharmacology)</term>
<term>Androstenediols (pharmacology)</term>
<term>Androstenols (pharmacology)</term>
<term>Animals</term>
<term>Concanavalin A (metabolism)</term>
<term>Dehydroepiandrosterone (pharmacology)</term>
<term>Glucocorticoids (antagonists & inhibitors)</term>
<term>Glucocorticoids (pharmacology)</term>
<term>Interleukin-2 (biosynthesis)</term>
<term>Interleukin-3 (biosynthesis)</term>
<term>Lipopolysaccharides (pharmacology)</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mitogens (pharmacology)</term>
<term>Spleen (cytology)</term>
<term>Spleen (drug effects)</term>
<term>Spleen (metabolism)</term>
<term>Thymidine (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Adjuvants immunologiques (pharmacologie)</term>
<term>Androstènediols (pharmacologie)</term>
<term>Androsténols (pharmacologie)</term>
<term>Animaux</term>
<term>Concanavaline A (métabolisme)</term>
<term>Déhydroépiandrostérone (pharmacologie)</term>
<term>Glucocorticoïdes (antagonistes et inhibiteurs)</term>
<term>Glucocorticoïdes (pharmacologie)</term>
<term>Interleukine-2 (biosynthèse)</term>
<term>Interleukine-3 (biosynthèse)</term>
<term>Lipopolysaccharides (pharmacologie)</term>
<term>Mitogènes (pharmacologie)</term>
<term>Rate ()</term>
<term>Rate (cytologie)</term>
<term>Rate (métabolisme)</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Thymidine (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Glucocorticoids</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Interleukin-2</term>
<term>Interleukin-3</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Concanavalin A</term>
<term>Thymidine</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Adjuvants, Immunologic</term>
<term>Androstenediols</term>
<term>Androstenols</term>
<term>Dehydroepiandrosterone</term>
<term>Glucocorticoids</term>
<term>Lipopolysaccharides</term>
<term>Mitogens</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Glucocorticoïdes</term>
</keywords>
<keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Interleukine-2</term>
<term>Interleukine-3</term>
</keywords>
<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Rate</term>
</keywords>
<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Spleen</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Spleen</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Spleen</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Concanavaline A</term>
<term>Rate</term>
<term>Thymidine</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Adjuvants immunologiques</term>
<term>Androstènediols</term>
<term>Androsténols</term>
<term>Déhydroépiandrostérone</term>
<term>Glucocorticoïdes</term>
<term>Lipopolysaccharides</term>
<term>Mitogènes</term>
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<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Rate</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
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<front><div type="abstract" xml:lang="en">The anti-inflammatory and immunosuppressive functions of corticosteroids have been well established and characterized. In contrast, a different group of native steroids, which include dehydroepiandrosterone (DHEA) and two of its metabolites, androstenediol (5-androstene-3 beta-17 beta-diol, AED) and androstenetriol (5-androstene-3 beta-7 beta-17 beta-triol, beta AET), function in vivo to up-regulate host immune response against infections and counteract stress-induced immunosuppression. Indeed, DHEA and particularly, AED and beta AET, have been shown to protect mice from viral, bacterial, and parasitic infections. In vivo, these three hormones are in opposition to the widely demonstrated immunosuppressive action of glucocorticoids, suggesting a possible new immune regulation mechanism. The individual activity in vitro of each of these steroids, i.e. DHEA, AED, and beta AET, on a mitogen-induced mixed splenocyte proliferation assay were determined. The results showed that DHEA suppressed the proliferation of cultures activated with concanavalin A (ConA) or lipopolysaccharide (LPS) in a dose-dependent manner. AED had little influence on the activation response. However, beta AET potentiated the response to both mitogens significantly above control. The regulation of the cytokine secretion, of both interleukin-2 (IL-2) and interleukin-3 (IL-3), from ConA-activated lymphocytes was affected in the same manner. These functions were depressed by DHEA, unaffected by AED, and potently increased by beta AET. Moreover, the classic immunosuppressive effects of hydrocortisone on ConA-induced lymphocyte proliferation, as well as on IL-2 and IL-3 production, were unaffected by being co-cultured with DHEA and only minimally counteracted by AED at high doses. In contrast, co-culturing with beta AET significantly counteracted the immunosuppressive effects of hydrocortisone on lymphocyte proliferation and cytokine production. These data show that in-vivo, DHEA, AED, and beta AET may have some similar functions, while in vitro, their effects are dramatically different from one another. Only beta AET could markedly potentiate the cellular response by increasing lymphocyte activation and counteracting the immnosuppressive activity of hydrocortisone on lymphocyte proliferation and cytokine production.</div>
</front>
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