IgA/IgM responses to tryptophan and tryptophan catabolites (TRYCATs) are differently associated with prenatal depression, physio-somatic symptoms at the end of term and premenstrual syndrome.
Identifieur interne : 000D39 ( PubMed/Curation ); précédent : 000D38; suivant : 000D40IgA/IgM responses to tryptophan and tryptophan catabolites (TRYCATs) are differently associated with prenatal depression, physio-somatic symptoms at the end of term and premenstrual syndrome.
Auteurs : Chutima Roomruangwong [Thaïlande] ; Buranee Kanchanatawan [Thaïlande] ; Sunee Sirivichayakul [Thaïlande] ; George Anderson [Royaume-Uni] ; André F. Carvalho [Brésil] ; Sebastien Duleu [France] ; Michel Geffard [France] ; Michael Maes [Thaïlande]Source :
- Molecular neurobiology [ 1559-1182 ] ; 2017.
Descripteurs français
- KwdFr :
- MESH :
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Immunoglobulin A, Immunoglobulin M, Tryptophan.
- metabolism : Depression, Postpartum, Premenstrual Syndrome.
- Adult, Female, Humans, Linear Models, Multivariate Analysis, Pregnancy, Principal Component Analysis.
Abstract
There is some evidence that lowered tryptophan and an activated tryptophan catabolite (TRYCAT) pathway play a role in depression, somatoform disorder, and postpartum blues. The aim of this study is to delineate the associations between the TRYCAT pathway and premenstrual syndrome (PMS) and perinatal depressive and physio-somatic symptoms. We examine the associations between end of term serum IgM and IgA responses to tryptophan and 9 TRYCATs in relation to zinc, C-reactive protein (CRP), and haptoglobin and prenatal physio-somatic (previously known as psychosomatic) symptoms (fatigue, back pain, muscle pain, dyspepsia, obstipation) and prenatal and postnatal depression and anxiety symptoms as measured using the Edinburgh Postnatal Depression Scale (EPDS), Hamilton Depression Rating Scale (HAMD), and Spielberger's State Anxiety Inventory (STAI). We included pregnant females with (n = 24) and without depression (n = 25) and 24 non-pregnant females. There were no significant associations between the IgA/IgM responses to tryptophan and TRYCATs and prenatal and postnatal depression/anxiety symptoms, except for lowered IgA responses to anthranilic acid in prenatal depression. A large part of the variance in IgA responses to most TRYCATs was explained by PMS and haptoglobin (positively) and CRP (inversely) levels. The IgA responses to TRYCATs were significantly increased in PMS, in particular picolinic, anthranilic, xanthurenic and kynurenic acid, and 3OH-kynurenine. Variance (62.5%) in physio-somatic symptoms at the end of term was explained by PMS, previous depressions, zinc (inversely), CRP and haptoglobin (both positively), and the IgM responses to quinolinic acid (positively), anthranilic acid, and tryptophan (both negatively). The results suggest that mucosa-derived TRYCAT pathway activation is significantly associated with PMS, but not with perinatal depression/anxiety symptoms. Physio-somatic symptoms in pregnancy have an immune-inflammatory pathophysiology. Induction of the TRYCAT pathway appears to be more related to physio-somatic than to depression symptoms.
DOI: 10.1007/s12035-016-9877-3
PubMed: 27037573
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">IgA/IgM responses to tryptophan and tryptophan catabolites (TRYCATs) are differently associated with prenatal depression, physio-somatic symptoms at the end of term and premenstrual syndrome.</title><author><name sortKey="Roomruangwong, Chutima" sort="Roomruangwong, Chutima" uniqKey="Roomruangwong C" first="Chutima" last="Roomruangwong">Chutima Roomruangwong</name><affiliation wicri:level="1"><nlm:affiliation>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.</nlm:affiliation><country xml:lang="fr">Thaïlande</country><wicri:regionArea>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok</wicri:regionArea></affiliation></author><author><name sortKey="Kanchanatawan, Buranee" sort="Kanchanatawan, Buranee" uniqKey="Kanchanatawan B" first="Buranee" last="Kanchanatawan">Buranee Kanchanatawan</name><affiliation wicri:level="1"><nlm:affiliation>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.</nlm:affiliation><country xml:lang="fr">Thaïlande</country><wicri:regionArea>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok</wicri:regionArea></affiliation></author><author><name sortKey="Sirivichayakul, Sunee" sort="Sirivichayakul, Sunee" uniqKey="Sirivichayakul S" first="Sunee" last="Sirivichayakul">Sunee Sirivichayakul</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.</nlm:affiliation><country xml:lang="fr">Thaïlande</country><wicri:regionArea>Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok</wicri:regionArea></affiliation></author><author><name sortKey="Anderson, George" sort="Anderson, George" uniqKey="Anderson G" first="George" last="Anderson">George Anderson</name><affiliation wicri:level="1"><nlm:affiliation>CRC Scotland and London, London, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>CRC Scotland and London, London</wicri:regionArea></affiliation></author><author><name sortKey="Carvalho, Andre F" sort="Carvalho, Andre F" uniqKey="Carvalho A" first="André F" last="Carvalho">André F. 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Carvalho</name><affiliation wicri:level="1"><nlm:affiliation>Department of Clinical Medicine and Translational Psychiatry Research Group, Faculty of Medicine, Federal University of Ceará, Fortaleza, CE, Brazil.</nlm:affiliation><country xml:lang="fr">Brésil</country><wicri:regionArea>Department of Clinical Medicine and Translational Psychiatry Research Group, Faculty of Medicine, Federal University of Ceará, Fortaleza, CE</wicri:regionArea></affiliation></author><author><name sortKey="Duleu, Sebastien" sort="Duleu, Sebastien" uniqKey="Duleu S" first="Sebastien" last="Duleu">Sebastien Duleu</name><affiliation wicri:level="1"><nlm:affiliation>Research Department, IDRPHT, Talence, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Research Department, IDRPHT, Talence</wicri:regionArea></affiliation></author><author><name sortKey="Geffard, Michel" sort="Geffard, Michel" uniqKey="Geffard M" first="Michel" last="Geffard">Michel Geffard</name><affiliation wicri:level="1"><nlm:affiliation>Research Department, IDRPHT, Talence, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Research Department, IDRPHT, Talence</wicri:regionArea></affiliation></author><author><name sortKey="Maes, Michael" sort="Maes, Michael" uniqKey="Maes M" first="Michael" last="Maes">Michael Maes</name><affiliation wicri:level="1"><nlm:affiliation>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand. dr.michaelmaes@hotmail.com.</nlm:affiliation><country xml:lang="fr">Thaïlande</country><wicri:regionArea>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok</wicri:regionArea></affiliation></author></analytic><series><title level="j">Molecular neurobiology</title><idno type="eISSN">1559-1182</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Depression, Postpartum (metabolism)</term><term>Female</term><term>Humans</term><term>Immunoglobulin A (metabolism)</term><term>Immunoglobulin M (metabolism)</term><term>Linear Models</term><term>Multivariate Analysis</term><term>Pregnancy</term><term>Premenstrual Syndrome (metabolism)</term><term>Principal Component Analysis</term><term>Tryptophan (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adulte</term><term>Analyse en composantes principales</term><term>Analyse multivariée</term><term>Dépression du postpartum (métabolisme)</term><term>Femelle</term><term>Grossesse</term><term>Humains</term><term>Immunoglobuline A (métabolisme)</term><term>Immunoglobuline M (métabolisme)</term><term>Modèles linéaires</term><term>Syndrome prémenstruel (métabolisme)</term><term>Tryptophane (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Immunoglobulin A</term><term>Immunoglobulin M</term><term>Tryptophan</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Depression, Postpartum</term><term>Premenstrual Syndrome</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Dépression du postpartum</term><term>Immunoglobuline A</term><term>Immunoglobuline M</term><term>Syndrome prémenstruel</term><term>Tryptophane</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Female</term><term>Humans</term><term>Linear Models</term><term>Multivariate Analysis</term><term>Pregnancy</term><term>Principal Component Analysis</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adulte</term><term>Analyse en composantes principales</term><term>Analyse multivariée</term><term>Femelle</term><term>Grossesse</term><term>Humains</term><term>Modèles linéaires</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">There is some evidence that lowered tryptophan and an activated tryptophan catabolite (TRYCAT) pathway play a role in depression, somatoform disorder, and postpartum blues. The aim of this study is to delineate the associations between the TRYCAT pathway and premenstrual syndrome (PMS) and perinatal depressive and physio-somatic symptoms. We examine the associations between end of term serum IgM and IgA responses to tryptophan and 9 TRYCATs in relation to zinc, C-reactive protein (CRP), and haptoglobin and prenatal physio-somatic (previously known as psychosomatic) symptoms (fatigue, back pain, muscle pain, dyspepsia, obstipation) and prenatal and postnatal depression and anxiety symptoms as measured using the Edinburgh Postnatal Depression Scale (EPDS), Hamilton Depression Rating Scale (HAMD), and Spielberger's State Anxiety Inventory (STAI). We included pregnant females with (n = 24) and without depression (n = 25) and 24 non-pregnant females. There were no significant associations between the IgA/IgM responses to tryptophan and TRYCATs and prenatal and postnatal depression/anxiety symptoms, except for lowered IgA responses to anthranilic acid in prenatal depression. A large part of the variance in IgA responses to most TRYCATs was explained by PMS and haptoglobin (positively) and CRP (inversely) levels. The IgA responses to TRYCATs were significantly increased in PMS, in particular picolinic, anthranilic, xanthurenic and kynurenic acid, and 3OH-kynurenine. Variance (62.5%) in physio-somatic symptoms at the end of term was explained by PMS, previous depressions, zinc (inversely), CRP and haptoglobin (both positively), and the IgM responses to quinolinic acid (positively), anthranilic acid, and tryptophan (both negatively). The results suggest that mucosa-derived TRYCAT pathway activation is significantly associated with PMS, but not with perinatal depression/anxiety symptoms. Physio-somatic symptoms in pregnancy have an immune-inflammatory pathophysiology. Induction of the TRYCAT pathway appears to be more related to physio-somatic than to depression symptoms.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27037573</PMID><DateCreated><Year>2016</Year><Month>04</Month><Day>02</Day></DateCreated><DateCompleted><Year>2017</Year><Month>07</Month><Day>07</Day></DateCompleted><DateRevised><Year>2017</Year><Month>07</Month><Day>18</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1559-1182</ISSN><JournalIssue CitedMedium="Internet"><Volume>54</Volume><Issue>4</Issue><PubDate><Year>2017</Year><Month>May</Month></PubDate></JournalIssue><Title>Molecular neurobiology</Title><ISOAbbreviation>Mol. Neurobiol.</ISOAbbreviation></Journal><ArticleTitle>IgA/IgM responses to tryptophan and tryptophan catabolites (TRYCATs) are differently associated with prenatal depression, physio-somatic symptoms at the end of term and premenstrual syndrome.</ArticleTitle><Pagination><MedlinePgn>3038-3049</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s12035-016-9877-3</ELocationID><Abstract><AbstractText>There is some evidence that lowered tryptophan and an activated tryptophan catabolite (TRYCAT) pathway play a role in depression, somatoform disorder, and postpartum blues. The aim of this study is to delineate the associations between the TRYCAT pathway and premenstrual syndrome (PMS) and perinatal depressive and physio-somatic symptoms. We examine the associations between end of term serum IgM and IgA responses to tryptophan and 9 TRYCATs in relation to zinc, C-reactive protein (CRP), and haptoglobin and prenatal physio-somatic (previously known as psychosomatic) symptoms (fatigue, back pain, muscle pain, dyspepsia, obstipation) and prenatal and postnatal depression and anxiety symptoms as measured using the Edinburgh Postnatal Depression Scale (EPDS), Hamilton Depression Rating Scale (HAMD), and Spielberger's State Anxiety Inventory (STAI). We included pregnant females with (n = 24) and without depression (n = 25) and 24 non-pregnant females. There were no significant associations between the IgA/IgM responses to tryptophan and TRYCATs and prenatal and postnatal depression/anxiety symptoms, except for lowered IgA responses to anthranilic acid in prenatal depression. A large part of the variance in IgA responses to most TRYCATs was explained by PMS and haptoglobin (positively) and CRP (inversely) levels. The IgA responses to TRYCATs were significantly increased in PMS, in particular picolinic, anthranilic, xanthurenic and kynurenic acid, and 3OH-kynurenine. Variance (62.5%) in physio-somatic symptoms at the end of term was explained by PMS, previous depressions, zinc (inversely), CRP and haptoglobin (both positively), and the IgM responses to quinolinic acid (positively), anthranilic acid, and tryptophan (both negatively). The results suggest that mucosa-derived TRYCAT pathway activation is significantly associated with PMS, but not with perinatal depression/anxiety symptoms. Physio-somatic symptoms in pregnancy have an immune-inflammatory pathophysiology. Induction of the TRYCAT pathway appears to be more related to physio-somatic than to depression symptoms.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Roomruangwong</LastName><ForeName>Chutima</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kanchanatawan</LastName><ForeName>Buranee</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sirivichayakul</LastName><ForeName>Sunee</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Anderson</LastName><ForeName>George</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>CRC Scotland and London, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Carvalho</LastName><ForeName>André F</ForeName><Initials>AF</Initials><AffiliationInfo><Affiliation>Department of Clinical Medicine and Translational Psychiatry Research Group, Faculty of Medicine, Federal University of Ceará, Fortaleza, CE, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Duleu</LastName><ForeName>Sebastien</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Research Department, IDRPHT, Talence, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Geffard</LastName><ForeName>Michel</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Research Department, IDRPHT, Talence, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>GEMAC, Lieu-Dit Berganton, Saint Jean d'Illac, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Maes</LastName><ForeName>Michael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand. dr.michaelmaes@hotmail.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Psychiatry, Faculty of Medicine, State University of Londrina, Londrina, Brazil. dr.michaelmaes@hotmail.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Psychiatry, Medical University Plovdiv, Plovdiv, Bulgaria. dr.michaelmaes@hotmail.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Revitalis, Waalre, The Netherlands. dr.michaelmaes@hotmail.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>IMPACT Research Center, Deakin University, Geelong, Australia. dr.michaelmaes@hotmail.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>IMPACT Strategic Research Center, Barwon Health, Deakin University, Geelong, VIC, Australia. dr.michaelmaes@hotmail.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>04</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mol Neurobiol</MedlineTA><NlmUniqueID>8900963</NlmUniqueID><ISSNLinking>0893-7648</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007070">Immunoglobulin A</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007075">Immunoglobulin M</NameOfSubstance></Chemical><Chemical><RegistryNumber>8DUH1N11BX</RegistryNumber><NameOfSubstance 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1;175(5):423-31</RefSource><PMID Version="1">22306563</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019052" MajorTopicYN="N">Depression, Postpartum</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007070" MajorTopicYN="N">Immunoglobulin A</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007075" MajorTopicYN="N">Immunoglobulin M</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016014" 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MajorTopicYN="N">Postnatal</Keyword><Keyword MajorTopicYN="N">Tryptophan</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>02</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>03</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>4</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>7</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>4</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27037573</ArticleId><ArticleId IdType="doi">10.1007/s12035-016-9877-3</ArticleId><ArticleId 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