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Sex differences in glucocorticoid sensitivity of proinflammatory cytokine production after psychosocial stress.

Identifieur interne : 000818 ( PubMed/Corpus ); précédent : 000817; suivant : 000819

Sex differences in glucocorticoid sensitivity of proinflammatory cytokine production after psychosocial stress.

Auteurs : N. Rohleder ; N C Schommer ; D H Hellhammer ; R. Engel ; C. Kirschbaum

Source :

RBID : pubmed:11719636

English descriptors

Abstract

Men and women show marked differences in susceptibility to disorders related to the immune system. These gender differences have been proposed to be mediated by functional interactions of the hypothalamus-pituitary-adrenal (HPA) and hypothalamus-pituitary-gonadal (HPG) axes. A potential mechanism involved in this interaction is the glucocorticoid (GC) sensitivity of relevant target tissues for GC. Therefore, the aim of the study reported here was to investigate the impact of psychosocial stress and HPA axis activation on the GC sensitivity of proinflammatory cytokine production in men and women.

PubMed: 11719636

Links to Exploration step

pubmed:11719636

Le document en format XML

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<name sortKey="Rohleder, N" sort="Rohleder, N" uniqKey="Rohleder N" first="N" last="Rohleder">N. Rohleder</name>
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<nlm:affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Trier, Germany.</nlm:affiliation>
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<name sortKey="Schommer, N C" sort="Schommer, N C" uniqKey="Schommer N" first="N C" last="Schommer">N C Schommer</name>
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<name sortKey="Hellhammer, D H" sort="Hellhammer, D H" uniqKey="Hellhammer D" first="D H" last="Hellhammer">D H Hellhammer</name>
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<name sortKey="Engel, R" sort="Engel, R" uniqKey="Engel R" first="R" last="Engel">R. Engel</name>
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<name sortKey="Kirschbaum, C" sort="Kirschbaum, C" uniqKey="Kirschbaum C" first="C" last="Kirschbaum">C. Kirschbaum</name>
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<term>Anti-Inflammatory Agents (pharmacokinetics)</term>
<term>Body Mass Index</term>
<term>Cytokines (biosynthesis)</term>
<term>Cytokines (immunology)</term>
<term>Dexamethasone (pharmacokinetics)</term>
<term>Female</term>
<term>Humans</term>
<term>Hydrocortisone (metabolism)</term>
<term>Hypothalamo-Hypophyseal System (metabolism)</term>
<term>Male</term>
<term>Pituitary-Adrenal System (metabolism)</term>
<term>Sex Factors</term>
<term>Stress Disorders, Post-Traumatic (immunology)</term>
<term>Stress Disorders, Post-Traumatic (metabolism)</term>
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<term>Cytokines</term>
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<term>Cytokines</term>
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<term>Hydrocortisone</term>
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<keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en">
<term>Anti-Inflammatory Agents</term>
<term>Dexamethasone</term>
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<keywords scheme="MESH" qualifier="immunology" xml:lang="en">
<term>Stress Disorders, Post-Traumatic</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en">
<term>Hypothalamo-Hypophyseal System</term>
<term>Pituitary-Adrenal System</term>
<term>Stress Disorders, Post-Traumatic</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Adult</term>
<term>Body Mass Index</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
<term>Sex Factors</term>
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<div type="abstract" xml:lang="en">Men and women show marked differences in susceptibility to disorders related to the immune system. These gender differences have been proposed to be mediated by functional interactions of the hypothalamus-pituitary-adrenal (HPA) and hypothalamus-pituitary-gonadal (HPG) axes. A potential mechanism involved in this interaction is the glucocorticoid (GC) sensitivity of relevant target tissues for GC. Therefore, the aim of the study reported here was to investigate the impact of psychosocial stress and HPA axis activation on the GC sensitivity of proinflammatory cytokine production in men and women.</div>
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<Year>2001</Year>
<Month>11</Month>
<Day>23</Day>
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<Year>2002</Year>
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<Volume>63</Volume>
<Issue>6</Issue>
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<MedlineDate>2001 Nov-Dec</MedlineDate>
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<Title>Psychosomatic medicine</Title>
<ISOAbbreviation>Psychosom Med</ISOAbbreviation>
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<ArticleTitle>Sex differences in glucocorticoid sensitivity of proinflammatory cytokine production after psychosocial stress.</ArticleTitle>
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<MedlinePgn>966-72</MedlinePgn>
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<Abstract>
<AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">Men and women show marked differences in susceptibility to disorders related to the immune system. These gender differences have been proposed to be mediated by functional interactions of the hypothalamus-pituitary-adrenal (HPA) and hypothalamus-pituitary-gonadal (HPG) axes. A potential mechanism involved in this interaction is the glucocorticoid (GC) sensitivity of relevant target tissues for GC. Therefore, the aim of the study reported here was to investigate the impact of psychosocial stress and HPA axis activation on the GC sensitivity of proinflammatory cytokine production in men and women.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">A total of 45 healthy subjects were investigated. Eighteen women in the luteal phase of their menstrual cycle and 27 men were exposed to a psychosocial stress test (Trier Social Stress Test). Salivary free cortisol levels were measured repeatedly after exposure to the stressor. GC sensitivity was assessed in vitro by dexamethasone inhibition of lipopolysaccharide-stimulated production of interleukin-6 and tumor necrosis factor-alpha.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">The stress test induced significant increases in salivary free cortisol with no significant differences between men and women. In contrast, GC sensitivity and lipopolysaccharide-stimulated cytokine production showed large gender differences. In men GC sensitivity was markedly increased 1 hour after stress, whereas GC sensitivity decreased significantly in women. Similarly, lipopolysaccharide-induced cytokine production decreased in response to stress in men but increased in women.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">These results demonstrate that despite similar free cortisol responses of men and women (studied in the luteal phase) to psychosocial stress, gender may exert differential effects on the immune system by modulating GC sensitivity of proinflammatory cytokine production.</AbstractText>
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