Endocrine and immune responses to stress in chronic inflammatory skin disorders.
Identifieur interne : 000777 ( PubMed/Corpus ); précédent : 000776; suivant : 000778Endocrine and immune responses to stress in chronic inflammatory skin disorders.
Auteurs : Angelika Buske-Kirschbaum ; Dirk H. HellhammerSource :
- Annals of the New York Academy of Sciences [ 0077-8923 ] ; 2003.
English descriptors
- KwdEn :
- Animals, Chronic Disease, Dermatitis, Atopic (immunology), Dermatitis, Atopic (physiopathology), Humans, Hypothalamo-Hypophyseal System (physiopathology), Inflammation (immunology), Inflammation (physiopathology), Pituitary-Adrenal System (physiopathology), Stress, Psychological (immunology), Stress, Psychological (physiopathology).
- MESH :
- immunology : Dermatitis, Atopic, Inflammation, Stress, Psychological.
- physiopathology : Dermatitis, Atopic, Hypothalamo-Hypophyseal System, Inflammation, Pituitary-Adrenal System, Stress, Psychological.
- Animals, Chronic Disease, Humans.
Abstract
Atopy is a genetically and environmentally determined condition predisposing to different forms such as atopic dermatitis (AD) or allergic asthma (AA). Both AD and AA are considered to be multifactorial diseases; however, distinct immunologic abnormalities have been described that play a crucial role. There is growing evidence that immunoglobulin-E hypersecretion and activation of the predominantly T-helper-2 (TH2)-like T cell subset trigger allergic inflammatory processes and cause the disease to become chronic. In the present paper, data suggesting reduced hypothalamic-pituitary-adrenal (HPA) axis responsiveness in patients with AD and AA are summarized, and the potential etiologic significance of a hyporeactive HPA axis is discussed. We propose that because of defective HPA axis, immunoregulation under stressful conditions is ineffective in patients with atopic conditions, leading to aberrant immune responses and subsequent exacerbation of the disease. Further research into the role of the HPA axis in atopy may elucidate the cause of stress-induced exacerbation of atopic symptoms and may be of clinical relevance.
PubMed: 12794062
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pubmed:12794062Le document en format XML
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Hellhammer</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2003">2003</date><idno type="RBID">pubmed:12794062</idno><idno type="pmid">12794062</idno><idno type="wicri:Area/PubMed/Corpus">000777</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000777</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Endocrine and immune responses to stress in chronic inflammatory skin disorders.</title><author><name sortKey="Buske Kirschbaum, Angelika" sort="Buske Kirschbaum, Angelika" uniqKey="Buske Kirschbaum A" first="Angelika" last="Buske-Kirschbaum">Angelika Buske-Kirschbaum</name><affiliation><nlm:affiliation>Department of Psychobiology, University of Trier, Trier, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Hellhammer, Dirk H" sort="Hellhammer, Dirk H" uniqKey="Hellhammer D" first="Dirk H" last="Hellhammer">Dirk H. Hellhammer</name></author></analytic><series><title level="j">Annals of the New York Academy of Sciences</title><idno type="ISSN">0077-8923</idno><imprint><date when="2003" type="published">2003</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Chronic Disease</term><term>Dermatitis, Atopic (immunology)</term><term>Dermatitis, Atopic (physiopathology)</term><term>Humans</term><term>Hypothalamo-Hypophyseal System (physiopathology)</term><term>Inflammation (immunology)</term><term>Inflammation (physiopathology)</term><term>Pituitary-Adrenal System (physiopathology)</term><term>Stress, Psychological (immunology)</term><term>Stress, Psychological (physiopathology)</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Dermatitis, Atopic</term><term>Inflammation</term><term>Stress, Psychological</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Dermatitis, Atopic</term><term>Hypothalamo-Hypophyseal System</term><term>Inflammation</term><term>Pituitary-Adrenal System</term><term>Stress, Psychological</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Chronic Disease</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Atopy is a genetically and environmentally determined condition predisposing to different forms such as atopic dermatitis (AD) or allergic asthma (AA). Both AD and AA are considered to be multifactorial diseases; however, distinct immunologic abnormalities have been described that play a crucial role. There is growing evidence that immunoglobulin-E hypersecretion and activation of the predominantly T-helper-2 (TH2)-like T cell subset trigger allergic inflammatory processes and cause the disease to become chronic. In the present paper, data suggesting reduced hypothalamic-pituitary-adrenal (HPA) axis responsiveness in patients with AD and AA are summarized, and the potential etiologic significance of a hyporeactive HPA axis is discussed. We propose that because of defective HPA axis, immunoregulation under stressful conditions is ineffective in patients with atopic conditions, leading to aberrant immune responses and subsequent exacerbation of the disease. Further research into the role of the HPA axis in atopy may elucidate the cause of stress-induced exacerbation of atopic symptoms and may be of clinical relevance.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12794062</PMID><DateCreated><Year>2003</Year><Month>06</Month><Day>09</Day></DateCreated><DateCompleted><Year>2003</Year><Month>07</Month><Day>07</Day></DateCompleted><DateRevised><Year>2006</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0077-8923</ISSN><JournalIssue CitedMedium="Print"><Volume>992</Volume><PubDate><Year>2003</Year><Month>May</Month></PubDate></JournalIssue><Title>Annals of the New York Academy of Sciences</Title><ISOAbbreviation>Ann. N. Y. Acad. Sci.</ISOAbbreviation></Journal><ArticleTitle>Endocrine and immune responses to stress in chronic inflammatory skin disorders.</ArticleTitle><Pagination><MedlinePgn>231-40</MedlinePgn></Pagination><Abstract><AbstractText>Atopy is a genetically and environmentally determined condition predisposing to different forms such as atopic dermatitis (AD) or allergic asthma (AA). Both AD and AA are considered to be multifactorial diseases; however, distinct immunologic abnormalities have been described that play a crucial role. There is growing evidence that immunoglobulin-E hypersecretion and activation of the predominantly T-helper-2 (TH2)-like T cell subset trigger allergic inflammatory processes and cause the disease to become chronic. In the present paper, data suggesting reduced hypothalamic-pituitary-adrenal (HPA) axis responsiveness in patients with AD and AA are summarized, and the potential etiologic significance of a hyporeactive HPA axis is discussed. We propose that because of defective HPA axis, immunoregulation under stressful conditions is ineffective in patients with atopic conditions, leading to aberrant immune responses and subsequent exacerbation of the disease. Further research into the role of the HPA axis in atopy may elucidate the cause of stress-induced exacerbation of atopic symptoms and may be of clinical relevance.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Buske-Kirschbaum</LastName><ForeName>Angelika</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Psychobiology, University of Trier, Trier, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hellhammer</LastName><ForeName>Dirk 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><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Ann N Y Acad Sci</MedlineTA><NlmUniqueID>7506858</NlmUniqueID><ISSNLinking>0077-8923</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002908" MajorTopicYN="N">Chronic Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003876" MajorTopicYN="N">Dermatitis, Atopic</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007030" MajorTopicYN="N">Hypothalamo-Hypophyseal System</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010913" MajorTopicYN="N">Pituitary-Adrenal System</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013315" MajorTopicYN="N">Stress, Psychological</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>42</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2003</Year><Month>6</Month><Day>10</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2003</Year><Month>7</Month><Day>8</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2003</Year><Month>6</Month><Day>10</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">12794062</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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