Stress-induced immunomodulation is altered in patients with atopic dermatitis.
Identifieur interne : 000799 ( PubMed/Corpus ); précédent : 000798; suivant : 000800Stress-induced immunomodulation is altered in patients with atopic dermatitis.
Auteurs : A. Buske-Kirschbaum ; A. Gierens ; H. Höllig ; D H HellhammerSource :
- Journal of neuroimmunology [ 0165-5728 ] ; 2002.
English descriptors
- KwdEn :
- Adjuvants, Immunologic (metabolism), Adult, Cytokines (metabolism), Dermatitis, Atopic (blood), Dermatitis, Atopic (immunology), Dermatitis, Atopic (psychology), Eosinophils (cytology), Eosinophils (immunology), Female, Humans, Immunoglobulin E (blood), Immunoglobulin E (immunology), Leukocyte Count, Leukocytes (cytology), Leukocytes (immunology), Male, Stress, Psychological (blood), Stress, Psychological (complications), Stress, Psychological (immunology), Up-Regulation (immunology).
- MESH :
- chemical , blood : Immunoglobulin E.
- chemical , immunology : Immunoglobulin E.
- chemical , metabolism : Adjuvants, Immunologic, Cytokines.
- blood : Dermatitis, Atopic, Stress, Psychological.
- complications : Stress, Psychological.
- cytology : Eosinophils, Leukocytes.
- immunology : Dermatitis, Atopic, Eosinophils, Leukocytes, Stress, Psychological, Up-Regulation.
- psychology : Dermatitis, Atopic.
- Adult, Female, Humans, Leukocyte Count, Male.
Abstract
Atopic dermatitis (AD) is a chronically relapsing inflammatory skin disease with main symptoms such as eczematous skin lesions and severe pruritus. Although the relevance of stress in the pathology of AD is widely accepted, the underlying biological mechanisms of stress-induced exacerbation of AD symptoms are not fully understood. The specific goal of the present study was to investigate the impact of acute psychosocial stress on atopy-relevant immune functions in AD sufferers. AD patients (n=36) and nonatopic controls (n=37) were exposed to a laboratory stressor including a free speech and mental arithmetic tasks in front of an audience ("Trier Social Stress Test," TSST). Blood samples were collected 10 min before and 1, 10 and 60 min after the stress test as well as 24 h after the experiment at identical time points under resting conditions. Analyses of leukocyte subsets indicated significantly elevated lymphocyte, monocyte, neutrophil and basophil numbers 10 min after the TSST (all p's<0.001) with no significant differences between the two groups. In contrast, eosinophil number was found to be significantly elevated only in AD sufferers, but not subjects (F(3,213)=4.8; p<0.01). Moreover, AD patients but not the control group showed increased IgE levels (F(1,71)=4.4; p<0.05) 24 h after the stress test. Exposure to the TSST resulted in elevation of interferon-gamma (IFN-gamma; F(3,207)=19.55; p<0.001) and, further, in attenuation of interleukin-4 (IL-4; F(3,207)=187.46; p<0.001) concentrations with no significant differences between both groups (all p's>0.05). The present findings suggest that stress may be associated with atopy-relevant immunological changes in AD sufferers, which may be one explanation of the common observation of stress-induced aggravation of symptomatology in this patient group.
PubMed: 12161032
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Stress-induced immunomodulation is altered in patients with atopic dermatitis.</title><author><name sortKey="Buske Kirschbaum, A" sort="Buske Kirschbaum, A" uniqKey="Buske Kirschbaum A" first="A" last="Buske-Kirschbaum">A. Buske-Kirschbaum</name><affiliation><nlm:affiliation>Department of Psychobiology, University of Trier, Universitätsring 1, 54286, Trier, Germany. buske@uni-trier.de</nlm:affiliation></affiliation></author><author><name sortKey="Gierens, A" sort="Gierens, A" uniqKey="Gierens A" first="A" last="Gierens">A. Gierens</name></author><author><name sortKey="Hollig, H" sort="Hollig, H" uniqKey="Hollig H" first="H" last="Höllig">H. Höllig</name></author><author><name sortKey="Hellhammer, D H" sort="Hellhammer, D H" uniqKey="Hellhammer D" first="D H" last="Hellhammer">D H Hellhammer</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2002">2002</date><idno type="RBID">pubmed:12161032</idno><idno type="pmid">12161032</idno><idno type="wicri:Area/PubMed/Corpus">000799</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000799</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Stress-induced immunomodulation is altered in patients with atopic dermatitis.</title><author><name sortKey="Buske Kirschbaum, A" sort="Buske Kirschbaum, A" uniqKey="Buske Kirschbaum A" first="A" last="Buske-Kirschbaum">A. Buske-Kirschbaum</name><affiliation><nlm:affiliation>Department of Psychobiology, University of Trier, Universitätsring 1, 54286, Trier, Germany. buske@uni-trier.de</nlm:affiliation></affiliation></author><author><name sortKey="Gierens, A" sort="Gierens, A" uniqKey="Gierens A" first="A" last="Gierens">A. Gierens</name></author><author><name sortKey="Hollig, H" sort="Hollig, H" uniqKey="Hollig H" first="H" last="Höllig">H. Höllig</name></author><author><name sortKey="Hellhammer, D H" sort="Hellhammer, D H" uniqKey="Hellhammer D" first="D H" last="Hellhammer">D H Hellhammer</name></author></analytic><series><title level="j">Journal of neuroimmunology</title><idno type="ISSN">0165-5728</idno><imprint><date when="2002" type="published">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adjuvants, Immunologic (metabolism)</term><term>Adult</term><term>Cytokines (metabolism)</term><term>Dermatitis, Atopic (blood)</term><term>Dermatitis, Atopic (immunology)</term><term>Dermatitis, Atopic (psychology)</term><term>Eosinophils (cytology)</term><term>Eosinophils (immunology)</term><term>Female</term><term>Humans</term><term>Immunoglobulin E (blood)</term><term>Immunoglobulin E (immunology)</term><term>Leukocyte Count</term><term>Leukocytes (cytology)</term><term>Leukocytes (immunology)</term><term>Male</term><term>Stress, Psychological (blood)</term><term>Stress, Psychological (complications)</term><term>Stress, Psychological (immunology)</term><term>Up-Regulation (immunology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Immunoglobulin E</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Immunoglobulin E</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adjuvants, Immunologic</term><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Dermatitis, Atopic</term><term>Stress, Psychological</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Stress, Psychological</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Eosinophils</term><term>Leukocytes</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Dermatitis, Atopic</term><term>Eosinophils</term><term>Leukocytes</term><term>Stress, Psychological</term><term>Up-Regulation</term></keywords><keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Dermatitis, Atopic</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Female</term><term>Humans</term><term>Leukocyte Count</term><term>Male</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Atopic dermatitis (AD) is a chronically relapsing inflammatory skin disease with main symptoms such as eczematous skin lesions and severe pruritus. Although the relevance of stress in the pathology of AD is widely accepted, the underlying biological mechanisms of stress-induced exacerbation of AD symptoms are not fully understood. The specific goal of the present study was to investigate the impact of acute psychosocial stress on atopy-relevant immune functions in AD sufferers. AD patients (n=36) and nonatopic controls (n=37) were exposed to a laboratory stressor including a free speech and mental arithmetic tasks in front of an audience ("Trier Social Stress Test," TSST). Blood samples were collected 10 min before and 1, 10 and 60 min after the stress test as well as 24 h after the experiment at identical time points under resting conditions. Analyses of leukocyte subsets indicated significantly elevated lymphocyte, monocyte, neutrophil and basophil numbers 10 min after the TSST (all p's<0.001) with no significant differences between the two groups. In contrast, eosinophil number was found to be significantly elevated only in AD sufferers, but not subjects (F(3,213)=4.8; p<0.01). Moreover, AD patients but not the control group showed increased IgE levels (F(1,71)=4.4; p<0.05) 24 h after the stress test. Exposure to the TSST resulted in elevation of interferon-gamma (IFN-gamma; F(3,207)=19.55; p<0.001) and, further, in attenuation of interleukin-4 (IL-4; F(3,207)=187.46; p<0.001) concentrations with no significant differences between both groups (all p's>0.05). The present findings suggest that stress may be associated with atopy-relevant immunological changes in AD sufferers, which may be one explanation of the common observation of stress-induced aggravation of symptomatology in this patient group.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12161032</PMID><DateCreated><Year>2002</Year><Month>08</Month><Day>05</Day></DateCreated><DateCompleted><Year>2002</Year><Month>09</Month><Day>27</Day></DateCompleted><DateRevised><Year>2009</Year><Month>11</Month><Day>03</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0165-5728</ISSN><JournalIssue CitedMedium="Print"><Volume>129</Volume><Issue>1-2</Issue><PubDate><Year>2002</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Journal of neuroimmunology</Title><ISOAbbreviation>J. Neuroimmunol.</ISOAbbreviation></Journal><ArticleTitle>Stress-induced immunomodulation is altered in patients with atopic dermatitis.</ArticleTitle><Pagination><MedlinePgn>161-7</MedlinePgn></Pagination><Abstract><AbstractText>Atopic dermatitis (AD) is a chronically relapsing inflammatory skin disease with main symptoms such as eczematous skin lesions and severe pruritus. Although the relevance of stress in the pathology of AD is widely accepted, the underlying biological mechanisms of stress-induced exacerbation of AD symptoms are not fully understood. The specific goal of the present study was to investigate the impact of acute psychosocial stress on atopy-relevant immune functions in AD sufferers. AD patients (n=36) and nonatopic controls (n=37) were exposed to a laboratory stressor including a free speech and mental arithmetic tasks in front of an audience ("Trier Social Stress Test," TSST). Blood samples were collected 10 min before and 1, 10 and 60 min after the stress test as well as 24 h after the experiment at identical time points under resting conditions. Analyses of leukocyte subsets indicated significantly elevated lymphocyte, monocyte, neutrophil and basophil numbers 10 min after the TSST (all p's<0.001) with no significant differences between the two groups. In contrast, eosinophil number was found to be significantly elevated only in AD sufferers, but not subjects (F(3,213)=4.8; p<0.01). Moreover, AD patients but not the control group showed increased IgE levels (F(1,71)=4.4; p<0.05) 24 h after the stress test. Exposure to the TSST resulted in elevation of interferon-gamma (IFN-gamma; F(3,207)=19.55; p<0.001) and, further, in attenuation of interleukin-4 (IL-4; F(3,207)=187.46; p<0.001) concentrations with no significant differences between both groups (all p's>0.05). The present findings suggest that stress may be associated with atopy-relevant immunological changes in AD sufferers, which may be one explanation of the common observation of stress-induced aggravation of symptomatology in this patient group.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Buske-Kirschbaum</LastName><ForeName>A</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Psychobiology, University of Trier, Universitätsring 1, 54286, Trier, Germany. buske@uni-trier.de</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gierens</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Höllig</LastName><ForeName>H</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Hellhammer</LastName><ForeName>D H</ForeName><Initials>DH</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>J Neuroimmunol</MedlineTA><NlmUniqueID>8109498</NlmUniqueID><ISSNLinking>0165-5728</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000276">Adjuvants, Immunologic</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>37341-29-0</RegistryNumber><NameOfSubstance UI="D007073">Immunoglobulin E</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000276" MajorTopicYN="N">Adjuvants, Immunologic</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003876" MajorTopicYN="N">Dermatitis, Atopic</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004804" MajorTopicYN="N">Eosinophils</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007073" MajorTopicYN="N">Immunoglobulin E</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007958" MajorTopicYN="N">Leukocyte Count</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007962" MajorTopicYN="N">Leukocytes</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013315" MajorTopicYN="N">Stress, Psychological</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015854" MajorTopicYN="N">Up-Regulation</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2002</Year><Month>8</Month><Day>6</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2002</Year><Month>9</Month><Day>28</Day><Hour>4</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2002</Year><Month>8</Month><Day>6</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">12161032</ArticleId><ArticleId IdType="pii">S0165572802001686</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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