Stress-induced neuroendocrine modulation of viral pathogenesis and immunity.
Identifieur interne : 000985 ( PubMed/Checkpoint ); précédent : 000984; suivant : 000986Stress-induced neuroendocrine modulation of viral pathogenesis and immunity.
Auteurs : J F Sheridan [États-Unis] ; C. Dobbs ; J. Jung ; X. Chu ; A. Konstantinos ; D. Padgett ; R. GlaserSource :
- Annals of the New York Academy of Sciences [ 0077-8923 ] ; 1998.
Descripteurs français
- KwdFr :
- MESH :
- immunologie : Maladies virales.
- physiologie : Immunité.
- physiopathologie : Stress physiologique, Système neuroendocrinien.
- étiologie : Maladies virales.
- Animaux, Humains.
English descriptors
- KwdEn :
- MESH :
- etiology : Virus Diseases.
- immunology : Virus Diseases.
- physiology : Immunity.
- physiopathology : Neurosecretory Systems, Stress, Physiological.
- Animals, Humans.
Abstract
Physical restraint (RST) was used to examine the interactions among the hypothalamic-pituitary-adrenal (HPA) axis, sympathetic nervous system, and the immune response to infection. In these studies, mice were infected with either herpes simplex virus (HSV) or influenza A/PR8 virus so that the impact of neuroendocrine activation could be assessed on disease pathophysiology and anti-viral immunity. RST suppressed lymphadenopathy in draining lymph nodes, reduced mononuclear cellular infiltration in the lungs, and suppressed virus-specific cytokine and cytolytic T-cell responses. Blockade of type II glucocorticoid receptors (by RU486) restored cellularity and cytokine responses to both organs in restraint-stressed, infected mice. Thus, the HPA axis modulated cell trafficking and T-cell cytokine responses. However, RU486 treatment failed to restore cytolytic T-cell responses. Blockade of beta-adrenergic receptors (by nadolol), in combination with RU486 treatment, fully restored cytolytic T-cell responses, suggesting that catecholamines were involved in suppressing the virus-specific CD8+ cytolytic T-cell response. RST also modulated the local development or expression of antibody-secreting cells (ASC) in the lungs draining lymph nodes, and spleen following infection of restrained mice. RST significantly suppressed the number of virus-specific ASC (IgM, IgG and subclasses IgG1 and IgG2a) in the lungs, mediastinal (MLN) lymph nodes and spleen, while it enhanced the responses in the superficial cervical (SCV) lymph nodes. This observation of differential modulation of ASC responses in the MLN and SCV lymph nodes supports the concept of tissue-specific immunoregulation in response to stress.
DOI: 10.1111/j.1749-6632.1998.tb09618.x
PubMed: 9629306
Affiliations:
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Glaser</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="1998" type="published">1998</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Humans</term><term>Immunity (physiology)</term><term>Neurosecretory Systems (physiopathology)</term><term>Stress, Physiological (physiopathology)</term><term>Virus Diseases (etiology)</term><term>Virus Diseases (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Immunité (physiologie)</term><term>Maladies virales (immunologie)</term><term>Maladies virales (étiologie)</term><term>Stress physiologique (physiopathologie)</term><term>Système neuroendocrinien (physiopathologie)</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Virus Diseases</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</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Immunity</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Stress physiologique</term><term>Système neuroendocrinien</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Neurosecretory Systems</term><term>Stress, Physiological</term></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Maladies virales</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Physical restraint (RST) was used to examine the interactions among the hypothalamic-pituitary-adrenal (HPA) axis, sympathetic nervous system, and the immune response to infection. In these studies, mice were infected with either herpes simplex virus (HSV) or influenza A/PR8 virus so that the impact of neuroendocrine activation could be assessed on disease pathophysiology and anti-viral immunity. RST suppressed lymphadenopathy in draining lymph nodes, reduced mononuclear cellular infiltration in the lungs, and suppressed virus-specific cytokine and cytolytic T-cell responses. Blockade of type II glucocorticoid receptors (by RU486) restored cellularity and cytokine responses to both organs in restraint-stressed, infected mice. Thus, the HPA axis modulated cell trafficking and T-cell cytokine responses. However, RU486 treatment failed to restore cytolytic T-cell responses. Blockade of beta-adrenergic receptors (by nadolol), in combination with RU486 treatment, fully restored cytolytic T-cell responses, suggesting that catecholamines were involved in suppressing the virus-specific CD8+ cytolytic T-cell response. RST also modulated the local development or expression of antibody-secreting cells (ASC) in the lungs draining lymph nodes, and spleen following infection of restrained mice. RST significantly suppressed the number of virus-specific ASC (IgM, IgG and subclasses IgG1 and IgG2a) in the lungs, mediastinal (MLN) lymph nodes and spleen, while it enhanced the responses in the superficial cervical (SCV) lymph nodes. This observation of differential modulation of ASC responses in the MLN and SCV lymph nodes supports the concept of tissue-specific immunoregulation in response to stress.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9629306</PMID><DateCompleted><Year>1998</Year><Month>07</Month><Day>09</Day></DateCompleted><DateRevised><Year>2019</Year><Month>06</Month><Day>16</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0077-8923</ISSN><JournalIssue CitedMedium="Print"><Volume>840</Volume><PubDate><Year>1998</Year><Month>May</Month><Day>01</Day></PubDate></JournalIssue><Title>Annals of the New York Academy of Sciences</Title><ISOAbbreviation>Ann. N. Y. Acad. Sci.</ISOAbbreviation></Journal><ArticleTitle>Stress-induced neuroendocrine modulation of viral pathogenesis and immunity.</ArticleTitle><Pagination><MedlinePgn>803-8</MedlinePgn></Pagination><Abstract><AbstractText>Physical restraint (RST) was used to examine the interactions among the hypothalamic-pituitary-adrenal (HPA) axis, sympathetic nervous system, and the immune response to infection. In these studies, mice were infected with either herpes simplex virus (HSV) or influenza A/PR8 virus so that the impact of neuroendocrine activation could be assessed on disease pathophysiology and anti-viral immunity. RST suppressed lymphadenopathy in draining lymph nodes, reduced mononuclear cellular infiltration in the lungs, and suppressed virus-specific cytokine and cytolytic T-cell responses. Blockade of type II glucocorticoid receptors (by RU486) restored cellularity and cytokine responses to both organs in restraint-stressed, infected mice. Thus, the HPA axis modulated cell trafficking and T-cell cytokine responses. However, RU486 treatment failed to restore cytolytic T-cell responses. Blockade of beta-adrenergic receptors (by nadolol), in combination with RU486 treatment, fully restored cytolytic T-cell responses, suggesting that catecholamines were involved in suppressing the virus-specific CD8+ cytolytic T-cell response. RST also modulated the local development or expression of antibody-secreting cells (ASC) in the lungs draining lymph nodes, and spleen following infection of restrained mice. RST significantly suppressed the number of virus-specific ASC (IgM, IgG and subclasses IgG1 and IgG2a) in the lungs, mediastinal (MLN) lymph nodes and spleen, while it enhanced the responses in the superficial cervical (SCV) lymph nodes. This observation of differential modulation of ASC responses in the MLN and SCV lymph nodes supports the concept of tissue-specific immunoregulation in response to stress.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sheridan</LastName><ForeName>J F</ForeName><Initials>JF</Initials><AffiliationInfo><Affiliation>Department of Oral Biology, College of Dentistry, Ohio State University Health Sciences Center, Columbus 43210, USA. sheridan.1@osu.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dobbs</LastName><ForeName>C</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Jung</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Chu</LastName><ForeName>X</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Konstantinos</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Padgett</LastName><ForeName>D</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Glaser</LastName><ForeName>R</ForeName><Initials>R</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01-MH46801</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 MH046801</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01-AG11585</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 MH018831</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32-MH18831</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</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="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007109" MajorTopicYN="N">Immunity</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009490" MajorTopicYN="N">Neurosecretory Systems</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013312" MajorTopicYN="N">Stress, Physiological</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014777" MajorTopicYN="N">Virus Diseases</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>20</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1998</Year><Month>6</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1998</Year><Month>6</Month><Day>18</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1998</Year><Month>6</Month><Day>18</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">9629306</ArticleId><ArticleId IdType="pmc">PMC1351103</ArticleId><ArticleId IdType="mid">NIHMS4566</ArticleId><ArticleId IdType="doi">10.1111/j.1749-6632.1998.tb09618.x</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>J Exp Med. 1984 Sep 1;160(3):814-26</Citation><ArticleIdList><ArticleId IdType="pubmed">6206190</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurosci Res. 1987;18(1):28-36, 118-21</Citation><ArticleIdList><ArticleId IdType="pubmed">3316680</ArticleId></ArticleIdList></Reference><Reference><Citation>Physiol Behav. 1989 Mar;45(3):591-4</Citation><ArticleIdList><ArticleId IdType="pubmed">2756050</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Immunol. 1991 Mar;133(1):234-52</Citation><ArticleIdList><ArticleId 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IdType="pubmed">8757304</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country></list><tree><noCountry><name sortKey="Chu, X" sort="Chu, X" uniqKey="Chu X" first="X" last="Chu">X. Chu</name><name sortKey="Dobbs, C" sort="Dobbs, C" uniqKey="Dobbs C" first="C" last="Dobbs">C. Dobbs</name><name sortKey="Glaser, R" sort="Glaser, R" uniqKey="Glaser R" first="R" last="Glaser">R. Glaser</name><name sortKey="Jung, J" sort="Jung, J" uniqKey="Jung J" first="J" last="Jung">J. Jung</name><name sortKey="Konstantinos, A" sort="Konstantinos, A" uniqKey="Konstantinos A" first="A" last="Konstantinos">A. Konstantinos</name><name sortKey="Padgett, D" sort="Padgett, D" uniqKey="Padgett D" first="D" last="Padgett">D. Padgett</name></noCountry><country name="États-Unis"><noRegion><name sortKey="Sheridan, J F" sort="Sheridan, J F" uniqKey="Sheridan J" first="J F" last="Sheridan">J F Sheridan</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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