Gut microbiome and innate immune response patterns in IgE-associated eczema.
Identifieur interne : 002B31 ( PubMed/Checkpoint ); précédent : 002B30; suivant : 002B32Gut microbiome and innate immune response patterns in IgE-associated eczema.
Auteurs : C E West [Suède] ; P. Rydén [Suède] ; D. Lundin [Suède] ; L. Engstrand [Suède] ; M K Tulic [Suède] ; S L Prescott [Suède]Source :
- Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology [ 1365-2222 ] ; 2015.
Descripteurs français
- KwdFr :
- Bactéries à Gram positif (), Bactéries à Gram positif (immunologie), Bactéries à Gram positif (isolement et purification), Eczéma atopique (immunologie), Eczéma atopique (microbiologie), Enfant d'âge préscolaire, Exposition maternelle (effets indésirables), Facteur de nécrose tumorale alpha (immunologie), Femelle, Grossesse, Humains, Immunité innée, Immunoglobuline E (immunologie), Interleukine-6 (immunologie), Intestins (immunologie), Intestins (microbiologie), Mâle, Nourrisson, Récepteur de type Toll-2 (immunologie), Récepteur de type Toll-4 (immunologie), Susceptibilité à une maladie.
- MESH :
- effets indésirables : Exposition maternelle.
- immunologie : Bactéries à Gram positif, Eczéma atopique, Facteur de nécrose tumorale alpha, Immunoglobuline E, Interleukine-6, Intestins, Récepteur de type Toll-2, Récepteur de type Toll-4.
- isolement et purification : Bactéries à Gram positif.
- microbiologie : Eczéma atopique, Intestins.
- Bactéries à Gram positif, Enfant d'âge préscolaire, Femelle, Grossesse, Humains, Immunité innée, Mâle, Nourrisson, Susceptibilité à une maladie.
English descriptors
- KwdEn :
- Child, Preschool, Dermatitis, Atopic (immunology), Dermatitis, Atopic (microbiology), Disease Susceptibility, Female, Gram-Positive Bacteria (classification), Gram-Positive Bacteria (immunology), Gram-Positive Bacteria (isolation & purification), Humans, Immunity, Innate, Immunoglobulin E (immunology), Infant, Interleukin-6 (immunology), Intestines (immunology), Intestines (microbiology), Male, Maternal Exposure (adverse effects), Pregnancy, Toll-Like Receptor 2 (immunology), Toll-Like Receptor 4 (immunology), Tumor Necrosis Factor-alpha (immunology).
- MESH :
- chemical , immunology : Immunoglobulin E, Interleukin-6, Toll-Like Receptor 2, Toll-Like Receptor 4, Tumor Necrosis Factor-alpha.
- adverse effects : Maternal Exposure.
- classification : Gram-Positive Bacteria.
- immunology : Dermatitis, Atopic, Gram-Positive Bacteria, Intestines.
- isolation & purification : Gram-Positive Bacteria.
- microbiology : Dermatitis, Atopic, Intestines.
- Child, Preschool, Disease Susceptibility, Female, Humans, Immunity, Innate, Infant, Male, Pregnancy.
Abstract
Gut microbiome patterns have been associated with predisposition to eczema potentially through modulation of innate immune signalling.
DOI: 10.1111/cea.12566
PubMed: 25944283
Affiliations:
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pubmed:25944283Le document en format XML
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(immunology)</term><term>Dermatitis, Atopic (microbiology)</term><term>Disease Susceptibility</term><term>Female</term><term>Gram-Positive Bacteria (classification)</term><term>Gram-Positive Bacteria (immunology)</term><term>Gram-Positive Bacteria (isolation & purification)</term><term>Humans</term><term>Immunity, Innate</term><term>Immunoglobulin E (immunology)</term><term>Infant</term><term>Interleukin-6 (immunology)</term><term>Intestines (immunology)</term><term>Intestines (microbiology)</term><term>Male</term><term>Maternal Exposure (adverse effects)</term><term>Pregnancy</term><term>Toll-Like Receptor 2 (immunology)</term><term>Toll-Like Receptor 4 (immunology)</term><term>Tumor Necrosis Factor-alpha (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Bactéries à Gram positif ()</term><term>Bactéries à Gram positif (immunologie)</term><term>Bactéries à Gram positif (isolement et purification)</term><term>Eczéma atopique (immunologie)</term><term>Eczéma atopique (microbiologie)</term><term>Enfant d'âge préscolaire</term><term>Exposition maternelle (effets indésirables)</term><term>Facteur de nécrose tumorale alpha (immunologie)</term><term>Femelle</term><term>Grossesse</term><term>Humains</term><term>Immunité innée</term><term>Immunoglobuline E (immunologie)</term><term>Interleukine-6 (immunologie)</term><term>Intestins (immunologie)</term><term>Intestins (microbiologie)</term><term>Mâle</term><term>Nourrisson</term><term>Récepteur de type Toll-2 (immunologie)</term><term>Récepteur de type Toll-4 (immunologie)</term><term>Susceptibilité à une maladie</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Immunoglobulin E</term><term>Interleukin-6</term><term>Toll-Like Receptor 2</term><term>Toll-Like Receptor 4</term><term>Tumor Necrosis Factor-alpha</term></keywords><keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Maternal Exposure</term></keywords><keywords scheme="MESH" qualifier="classification" xml:lang="en"><term>Gram-Positive Bacteria</term></keywords><keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Exposition maternelle</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Bactéries à Gram positif</term><term>Eczéma atopique</term><term>Facteur de nécrose tumorale alpha</term><term>Immunoglobuline E</term><term>Interleukine-6</term><term>Intestins</term><term>Récepteur de type Toll-2</term><term>Récepteur de type Toll-4</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Dermatitis, Atopic</term><term>Gram-Positive Bacteria</term><term>Intestines</term></keywords><keywords scheme="MESH" qualifier="isolation & purification" xml:lang="en"><term>Gram-Positive Bacteria</term></keywords><keywords scheme="MESH" qualifier="isolement et purification" xml:lang="fr"><term>Bactéries à Gram positif</term></keywords><keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Eczéma atopique</term><term>Intestins</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Dermatitis, Atopic</term><term>Intestines</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Child, Preschool</term><term>Disease Susceptibility</term><term>Female</term><term>Humans</term><term>Immunity, Innate</term><term>Infant</term><term>Male</term><term>Pregnancy</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Bactéries à Gram positif</term><term>Enfant d'âge préscolaire</term><term>Femelle</term><term>Grossesse</term><term>Humains</term><term>Immunité innée</term><term>Mâle</term><term>Nourrisson</term><term>Susceptibilité à une maladie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Gut microbiome patterns have been associated with predisposition to eczema potentially through modulation of innate immune signalling.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25944283</PMID><DateCreated><Year>2015</Year><Month>08</Month><Day>24</Day></DateCreated><DateCompleted><Year>2016</Year><Month>05</Month><Day>13</Day></DateCompleted><DateRevised><Year>2015</Year><Month>08</Month><Day>24</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1365-2222</ISSN><JournalIssue CitedMedium="Internet"><Volume>45</Volume><Issue>9</Issue><PubDate><Year>2015</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology</Title><ISOAbbreviation>Clin. Exp. Allergy</ISOAbbreviation></Journal><ArticleTitle>Gut microbiome and innate immune response patterns in IgE-associated eczema.</ArticleTitle><Pagination><MedlinePgn>1419-29</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/cea.12566</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Gut microbiome patterns have been associated with predisposition to eczema potentially through modulation of innate immune signalling.</AbstractText><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">We examined gut microbiome development in the first year of life in relation to innate immune responses and onset of IgE-associated eczema over the first 2.5 years in predisposed children due to maternal atopy [www.anzctr.org.au, trial ID ACTRN12606000280505].</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Microbial composition and diversity were analysed with barcoded 16S rRNA 454 pyrosequencing in stool samples in pregnancy and at ages 1 week, 1 month and 12 months in infants (n = 10) who developed IgE-associated eczema and infants who remained free of any allergic symptoms at 2.5 years of age (n = 10). Microbiome data at 1 week and 1 month were analysed in relation to previously assessed immune responses to TLR 2 and 4 ligands at 6 months of age.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">The relative abundance of Gram-positive Ruminococcaceae was lower at 1 week of age in infants developing IgE-associated eczema, compared with controls (P = 0.0047). At that age, the relative abundance of Ruminococcus was inversely associated with TLR2 induced IL-6 (-0.567, P = 0.042) and TNF-α (-0.597, P = 0.032); there was also an inverse association between the abundance of Proteobacteria (comprising Gram-negative taxa) and TLR4-induced TNF-α (rs = -0.629, P = 0.024). This relationship persisted at 1 month, with inverse associations between the relative abundance of Enterobacteriaceae (within the Proteobacteria phylum) and TLR4-induced TNF-α (rs = -0.697, P = 0.038) and Enterobacteriaceae and IL-6 (rs = -0.709, P = 0.035). Mothers whose infants developed IgE-associated eczema had lower α-diversity of Bacteroidetes (P = 0.04) although this was not seen later in their infants. At 1 year, α-diversity of Actinobacteria was lower in infants with IgE-associated eczema compared with controls (P = 0.002).</AbstractText><AbstractText Label="CONCLUSION AND CLINICAL RELEVANCE" NlmCategory="CONCLUSIONS">Our findings suggest that reduced relative abundance of potentially immunomodulatory gut bacteria is associated with exaggerated inflammatory cytokine responses to TLR-ligands and subsequent development of IgE-associated eczema.</AbstractText><CopyrightInformation>© 2015 John Wiley & Sons Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>West</LastName><ForeName>C E</ForeName><Initials>CE</Initials><AffiliationInfo><Affiliation>International Inflammation Network (in-FLAME) of the World Universities Network, Umeå, Sweden.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Clinical Sciences, Pediatrics, Umeå University, Umeå, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rydén</LastName><ForeName>P</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Mathematics and Mathematical Statistics, Umeå University, Umeå, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lundin</LastName><ForeName>D</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Tumor and Cell Biology, Science for Life Laboratory, Karolinska Institutet, Stockholm, Sweden.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Bioinformatics Infrastructure for Life Sciences, Science for Life Laboratory, Stockholm, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Engstrand</LastName><ForeName>L</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Tumor and Cell Biology, Science for Life Laboratory, Karolinska Institutet, Stockholm, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tulic</LastName><ForeName>M K</ForeName><Initials>MK</Initials><AffiliationInfo><Affiliation>International Inflammation Network (in-FLAME) of the World Universities Network, Umeå, Sweden.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Université de Nice Sophia-Antipolis, Nice, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Prescott</LastName><ForeName>S L</ForeName><Initials>SL</Initials><AffiliationInfo><Affiliation>International Inflammation Network (in-FLAME) of the World Universities Network, Umeå, Sweden.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Paediatrics and Child Health, University of Western Australia, Perth, Australia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016430">Clinical Trial</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Clin Exp Allergy</MedlineTA><NlmUniqueID>8906443</NlmUniqueID><ISSNLinking>0954-7894</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C508600">IL6 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015850">Interleukin-6</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C495342">TLR2 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C495345">TLR4 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051195">Toll-Like Receptor 2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051197">Toll-Like Receptor 4</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014409">Tumor Necrosis Factor-alpha</NameOfSubstance></Chemical><Chemical><RegistryNumber>37341-29-0</RegistryNumber><NameOfSubstance UI="D007073">Immunoglobulin E</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D002675" MajorTopicYN="N">Child, Preschool</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003876" MajorTopicYN="N">Dermatitis, Atopic</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004198" MajorTopicYN="N">Disease Susceptibility</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006094" MajorTopicYN="N">Gram-Positive Bacteria</DescriptorName><QualifierName UI="Q000145" MajorTopicYN="N">classification</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000302" MajorTopicYN="N">isolation & purification</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007113" MajorTopicYN="Y">Immunity, Innate</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007073" MajorTopicYN="N">Immunoglobulin E</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007223" MajorTopicYN="N">Infant</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015850" MajorTopicYN="N">Interleukin-6</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007422" MajorTopicYN="N">Intestines</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018811" MajorTopicYN="N">Maternal Exposure</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011247" MajorTopicYN="N">Pregnancy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051195" MajorTopicYN="N">Toll-Like Receptor 2</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051197" MajorTopicYN="N">Toll-Like Receptor 4</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014409" 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PubStatus="entrez"><Year>2015</Year><Month>5</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>5</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>5</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25944283</ArticleId><ArticleId IdType="doi">10.1111/cea.12566</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Suède</li></country><region><li>Svealand</li></region><settlement><li>Stockholm</li></settlement></list><tree><country name="Suède"><noRegion><name sortKey="West, C E" sort="West, C E" uniqKey="West C" first="C E" last="West">C E West</name></noRegion><name sortKey="Engstrand, L" sort="Engstrand, L" uniqKey="Engstrand L" first="L" last="Engstrand">L. Engstrand</name><name sortKey="Lundin, D" sort="Lundin, D" uniqKey="Lundin D" first="D" last="Lundin">D. Lundin</name><name sortKey="Prescott, S L" sort="Prescott, S L" uniqKey="Prescott S" first="S L" last="Prescott">S L Prescott</name><name sortKey="Ryden, P" sort="Ryden, P" uniqKey="Ryden P" first="P" last="Rydén">P. Rydén</name><name sortKey="Tulic, M K" sort="Tulic, M K" uniqKey="Tulic M" first="M K" last="Tulic">M K Tulic</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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