A Mutation in IL4RA Is Associated with the Degree of Pathology in Human TB Patients.
Identifieur interne : 000167 ( PubMed/Checkpoint ); précédent : 000166; suivant : 000168A Mutation in IL4RA Is Associated with the Degree of Pathology in Human TB Patients.
Auteurs : Christoph Hölscher [Allemagne] ; Lisa Heitmann [Allemagne] ; Ellis Owusu-Dabo [Ghana] ; Rolf D. Horstmann [Allemagne] ; Christian G. Meyer [Allemagne] ; Stefan Ehlers [Allemagne] ; Thorsten Thye [Allemagne]Source :
- Mediators of inflammation [ 1466-1861 ] ; 2016.
Descripteurs français
- KwdFr :
- Animaux, Femelle, Ghana, Humains, Interleukine-13 (métabolisme), Interleukine-4 (métabolisme), Mutation, Mâle, Souris, Souris transgéniques, Sous-unité alpha du récepteur à l'interleukine-4 (génétique), Sous-unité alpha2 du récepteur à l'interleukine-13 (métabolisme), Transduction du signal (génétique), Transduction du signal (physiologie), Tuberculose pulmonaire (génétique).
- MESH :
- génétique : Sous-unité alpha du récepteur à l'interleukine-4, Transduction du signal, Tuberculose pulmonaire.
- métabolisme : Interleukine-13, Interleukine-4, Sous-unité alpha2 du récepteur à l'interleukine-13.
- physiologie : Transduction du signal.
- Animaux, Femelle, Ghana, Humains, Mutation, Mâle, Souris, Souris transgéniques.
English descriptors
- KwdEn :
- Animals, Female, Ghana, Humans, Interleukin-13 (metabolism), Interleukin-13 Receptor alpha2 Subunit (metabolism), Interleukin-4 (metabolism), Interleukin-4 Receptor alpha Subunit (genetics), Male, Mice, Mice, Transgenic, Mutation, Signal Transduction (genetics), Signal Transduction (physiology), Tuberculosis, Pulmonary (genetics).
- MESH :
- chemical , genetics : Interleukin-4 Receptor alpha Subunit.
- chemical , metabolism : Interleukin-13, Interleukin-13 Receptor alpha2 Subunit, Interleukin-4.
- genetics : Signal Transduction, Tuberculosis, Pulmonary.
- physiology : Signal Transduction.
- Animals, Female, Ghana, Humans, Male, Mice, Mice, Transgenic, Mutation.
Abstract
The contribution of interleukin- (IL-) 4 receptor-alpha- (Rα-) dependent events in the pathogenesis of tuberculosis (TB) is controversial. We have recently shown IL-13 overexpression in mice to cause recrudescent Mtb replication and centrally necrotizing granulomas strongly resembling pathology of human TB. A deletion of IL-4Rα completely abrogates TB tissue pathology in these mice. To validate our results in human TB patients, we here determined the association of distinct variants of the IL4, IL13, IL4RA, IL13RA1, and IL13RA2 genes with cavity formation in a large Ghanaian cohort of HIV-negative individuals with newly diagnosed pulmonary TB. In fact, the structural variant of the IL4RA I50V, previously shown to result in enhanced signal transduction, was significantly associated with greater cavity size, and a variant of IL13RA2 was associated with disease in females. To evaluate whether the human-like TB pathology in IL-13-overexpressing mice is specifically mediated through the IL-4Rα subunit, we analyzed IL-13 transgenic mice with a genetic ablation of the IL-4Rα. In these mice, the IL-13-mediated increased susceptibility, human-like pathology of collagen deposition around centrally necrotizing granulomas, and alternative macrophage activation were abolished. Together, our genetic association study in human TB patients further supports the assumption that IL-13/IL-4Rα-dependent mechanisms are involved in mediating tissue pathology of human TB.
DOI: 10.1155/2016/4245028
PubMed: 26977119
Affiliations:
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German Center for Infection Research, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Infection Immunology, Research Center Borstel, Parkallee 22, 23845 Borstel, Germany; German Center for Infection Research</wicri:regionArea><wicri:noRegion>Germany; German Center for Infection Research</wicri:noRegion><wicri:noRegion>Germany; German Center for Infection Research</wicri:noRegion><wicri:noRegion>Germany; German Center for Infection Research</wicri:noRegion></affiliation></author><author><name sortKey="Heitmann, Lisa" sort="Heitmann, Lisa" uniqKey="Heitmann L" first="Lisa" last="Heitmann">Lisa Heitmann</name><affiliation wicri:level="1"><nlm:affiliation>Infection Immunology, Research Center Borstel, Parkallee 22, 23845 Borstel, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Infection Immunology, Research Center Borstel, Parkallee 22, 23845 Borstel</wicri:regionArea><wicri:noRegion>23845 Borstel</wicri:noRegion><wicri:noRegion>23845 Borstel</wicri:noRegion><wicri:noRegion>23845 Borstel</wicri:noRegion></affiliation></author><author><name sortKey="Owusu Dabo, Ellis" sort="Owusu Dabo, Ellis" uniqKey="Owusu Dabo E" first="Ellis" last="Owusu-Dabo">Ellis Owusu-Dabo</name><affiliation wicri:level="1"><nlm:affiliation>Department of Community Health, College of Health Sciences, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana.</nlm:affiliation><country xml:lang="fr">Ghana</country><wicri:regionArea>Department of Community Health, College of Health Sciences, Kwame Nkrumah University of Science and Technology, Kumasi</wicri:regionArea><wicri:noRegion>Kumasi</wicri:noRegion></affiliation></author><author><name sortKey="Horstmann, Rolf D" sort="Horstmann, Rolf D" uniqKey="Horstmann R" first="Rolf D" last="Horstmann">Rolf D. Horstmann</name><affiliation wicri:level="1"><nlm:affiliation>German Center for Infection Research, Germany; Department of Molecular Medicine, Bernhard Nocht Institute for Tropical Medicine, Bernhard-Nocht-Strasse 74, 20359 Hamburg, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>German Center for Infection Research, Germany; Department of Molecular Medicine, Bernhard Nocht Institute for Tropical Medicine, Bernhard-Nocht-Strasse 74, 20359 Hamburg</wicri:regionArea><wicri:noRegion>20359 Hamburg</wicri:noRegion><placeName><settlement type="city">Hambourg</settlement><region type="land" nuts="2">Hambourg</region></placeName></affiliation></author><author><name sortKey="Meyer, Christian G" sort="Meyer, Christian G" uniqKey="Meyer C" first="Christian G" last="Meyer">Christian G. Meyer</name><affiliation wicri:level="1"><nlm:affiliation>German Center for Infection Research, Germany; Department of Molecular Medicine, Bernhard Nocht Institute for Tropical Medicine, Bernhard-Nocht-Strasse 74, 20359 Hamburg, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>German Center for Infection Research, Germany; Department of Molecular Medicine, Bernhard Nocht Institute for Tropical Medicine, Bernhard-Nocht-Strasse 74, 20359 Hamburg</wicri:regionArea><wicri:noRegion>20359 Hamburg</wicri:noRegion><placeName><settlement type="city">Hambourg</settlement><region type="land" nuts="2">Hambourg</region></placeName></affiliation></author><author><name sortKey="Ehlers, Stefan" sort="Ehlers, Stefan" uniqKey="Ehlers S" first="Stefan" last="Ehlers">Stefan Ehlers</name><affiliation wicri:level="3"><nlm:affiliation>German Center for Infection Research, Germany; Microbial Inflammation Research, Research Center Borstel, Parkallee 22, 23845 Borstel, Germany; Molecular Inflammation Medicine, Christian Albrechts University, Christian-Albrechts-Platz 4, 24098 Kiel, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>German Center for Infection Research, Germany; Microbial Inflammation Research, Research Center Borstel, Parkallee 22, 23845 Borstel, Germany; Molecular Inflammation Medicine, Christian Albrechts University, Christian-Albrechts-Platz 4, 24098 Kiel</wicri:regionArea><placeName><region type="land" nuts="2">Schleswig-Holstein</region><settlement type="city">Kiel</settlement></placeName></affiliation></author><author><name sortKey="Thye, Thorsten" sort="Thye, Thorsten" uniqKey="Thye T" first="Thorsten" last="Thye">Thorsten Thye</name><affiliation wicri:level="1"><nlm:affiliation>German Center for Infection Research, Germany; Department of Molecular Medicine, Bernhard Nocht Institute for Tropical Medicine, Bernhard-Nocht-Strasse 74, 20359 Hamburg, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>German Center for Infection Research, Germany; Department of Molecular Medicine, Bernhard Nocht Institute for Tropical Medicine, Bernhard-Nocht-Strasse 74, 20359 Hamburg</wicri:regionArea><wicri:noRegion>20359 Hamburg</wicri:noRegion><placeName><settlement type="city">Hambourg</settlement><region type="land" nuts="2">Hambourg</region></placeName></affiliation></author></analytic><series><title level="j">Mediators of inflammation</title><idno type="eISSN">1466-1861</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Female</term><term>Ghana</term><term>Humans</term><term>Interleukin-13 (metabolism)</term><term>Interleukin-13 Receptor alpha2 Subunit (metabolism)</term><term>Interleukin-4 (metabolism)</term><term>Interleukin-4 Receptor alpha Subunit (genetics)</term><term>Male</term><term>Mice</term><term>Mice, Transgenic</term><term>Mutation</term><term>Signal Transduction (genetics)</term><term>Signal Transduction (physiology)</term><term>Tuberculosis, Pulmonary (genetics)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Femelle</term><term>Ghana</term><term>Humains</term><term>Interleukine-13 (métabolisme)</term><term>Interleukine-4 (métabolisme)</term><term>Mutation</term><term>Mâle</term><term>Souris</term><term>Souris transgéniques</term><term>Sous-unité alpha du récepteur à l'interleukine-4 (génétique)</term><term>Sous-unité alpha2 du récepteur à l'interleukine-13 (métabolisme)</term><term>Transduction du signal (génétique)</term><term>Transduction du signal (physiologie)</term><term>Tuberculose pulmonaire (génétique)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Interleukin-4 Receptor alpha Subunit</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Interleukin-13</term><term>Interleukin-13 Receptor alpha2 Subunit</term><term>Interleukin-4</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Signal Transduction</term><term>Tuberculosis, Pulmonary</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Sous-unité alpha du récepteur à l'interleukine-4</term><term>Transduction du signal</term><term>Tuberculose pulmonaire</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Interleukine-13</term><term>Interleukine-4</term><term>Sous-unité alpha2 du récepteur à l'interleukine-13</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Transduction du signal</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Female</term><term>Ghana</term><term>Humans</term><term>Male</term><term>Mice</term><term>Mice, Transgenic</term><term>Mutation</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Femelle</term><term>Ghana</term><term>Humains</term><term>Mutation</term><term>Mâle</term><term>Souris</term><term>Souris transgéniques</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The contribution of interleukin- (IL-) 4 receptor-alpha- (Rα-) dependent events in the pathogenesis of tuberculosis (TB) is controversial. We have recently shown IL-13 overexpression in mice to cause recrudescent Mtb replication and centrally necrotizing granulomas strongly resembling pathology of human TB. A deletion of IL-4Rα completely abrogates TB tissue pathology in these mice. To validate our results in human TB patients, we here determined the association of distinct variants of the IL4, IL13, IL4RA, IL13RA1, and IL13RA2 genes with cavity formation in a large Ghanaian cohort of HIV-negative individuals with newly diagnosed pulmonary TB. In fact, the structural variant of the IL4RA I50V, previously shown to result in enhanced signal transduction, was significantly associated with greater cavity size, and a variant of IL13RA2 was associated with disease in females. To evaluate whether the human-like TB pathology in IL-13-overexpressing mice is specifically mediated through the IL-4Rα subunit, we analyzed IL-13 transgenic mice with a genetic ablation of the IL-4Rα. In these mice, the IL-13-mediated increased susceptibility, human-like pathology of collagen deposition around centrally necrotizing granulomas, and alternative macrophage activation were abolished. Together, our genetic association study in human TB patients further supports the assumption that IL-13/IL-4Rα-dependent mechanisms are involved in mediating tissue pathology of human TB.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26977119</PMID><DateCreated><Year>2016</Year><Month>03</Month><Day>15</Day></DateCreated><DateCompleted><Year>2016</Year><Month>12</Month><Day>13</Day></DateCompleted><DateRevised><Year>2016</Year><Month>12</Month><Day>30</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1466-1861</ISSN><JournalIssue CitedMedium="Internet"><Volume>2016</Volume><PubDate><Year>2016</Year></PubDate></JournalIssue><Title>Mediators of inflammation</Title><ISOAbbreviation>Mediators Inflamm.</ISOAbbreviation></Journal><ArticleTitle>A Mutation in IL4RA Is Associated with the Degree of Pathology in Human TB Patients.</ArticleTitle><Pagination><MedlinePgn>4245028</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1155/2016/4245028</ELocationID><Abstract><AbstractText>The contribution of interleukin- (IL-) 4 receptor-alpha- (Rα-) dependent events in the pathogenesis of tuberculosis (TB) is controversial. We have recently shown IL-13 overexpression in mice to cause recrudescent Mtb replication and centrally necrotizing granulomas strongly resembling pathology of human TB. A deletion of IL-4Rα completely abrogates TB tissue pathology in these mice. To validate our results in human TB patients, we here determined the association of distinct variants of the IL4, IL13, IL4RA, IL13RA1, and IL13RA2 genes with cavity formation in a large Ghanaian cohort of HIV-negative individuals with newly diagnosed pulmonary TB. In fact, the structural variant of the IL4RA I50V, previously shown to result in enhanced signal transduction, was significantly associated with greater cavity size, and a variant of IL13RA2 was associated with disease in females. To evaluate whether the human-like TB pathology in IL-13-overexpressing mice is specifically mediated through the IL-4Rα subunit, we analyzed IL-13 transgenic mice with a genetic ablation of the IL-4Rα. In these mice, the IL-13-mediated increased susceptibility, human-like pathology of collagen deposition around centrally necrotizing granulomas, and alternative macrophage activation were abolished. Together, our genetic association study in human TB patients further supports the assumption that IL-13/IL-4Rα-dependent mechanisms are involved in mediating tissue pathology of human TB.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hölscher</LastName><ForeName>Christoph</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Infection Immunology, Research Center Borstel, Parkallee 22, 23845 Borstel, Germany; German Center for Infection Research, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Heitmann</LastName><ForeName>Lisa</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Infection Immunology, Research Center Borstel, Parkallee 22, 23845 Borstel, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Owusu-Dabo</LastName><ForeName>Ellis</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Community Health, College of Health Sciences, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Horstmann</LastName><ForeName>Rolf D</ForeName><Initials>RD</Initials><AffiliationInfo><Affiliation>German Center for Infection Research, Germany; Department of Molecular Medicine, Bernhard Nocht Institute for Tropical Medicine, Bernhard-Nocht-Strasse 74, 20359 Hamburg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Meyer</LastName><ForeName>Christian G</ForeName><Initials>CG</Initials><AffiliationInfo><Affiliation>German Center for Infection Research, Germany; Department of Molecular Medicine, Bernhard Nocht Institute for Tropical Medicine, Bernhard-Nocht-Strasse 74, 20359 Hamburg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ehlers</LastName><ForeName>Stefan</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>German Center for Infection Research, Germany; Microbial Inflammation Research, Research Center Borstel, Parkallee 22, 23845 Borstel, Germany; Molecular Inflammation Medicine, Christian Albrechts University, Christian-Albrechts-Platz 4, 24098 Kiel, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Thye</LastName><ForeName>Thorsten</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>German Center for Infection Research, Germany; Department of Molecular Medicine, Bernhard Nocht Institute for Tropical Medicine, Bernhard-Nocht-Strasse 74, 20359 Hamburg, Germany.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>02</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mediators Inflamm</MedlineTA><NlmUniqueID>9209001</NlmUniqueID><ISSNLinking>0962-9351</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018793">Interleukin-13</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053663">Interleukin-13 Receptor alpha2 Subunit</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053662">Interleukin-4 Receptor alpha Subunit</NameOfSubstance></Chemical><Chemical><RegistryNumber>207137-56-2</RegistryNumber><NameOfSubstance UI="D015847">Interleukin-4</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>J Rheumatol. 2006 Oct;33(10):2015-9</RefSource><PMID Version="1">16981293</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Infect Dis. 2006 Nov 15;194(10):1385-93</RefSource><PMID 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MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014397" MajorTopicYN="N">Tuberculosis, Pulmonary</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC4764744</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>10</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>01</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>3</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>3</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>12</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26977119</ArticleId><ArticleId IdType="doi">10.1155/2016/4245028</ArticleId><ArticleId IdType="pmc">PMC4764744</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li><li>Ghana</li></country><region><li>Hambourg</li><li>Schleswig-Holstein</li></region><settlement><li>Hambourg</li><li>Kiel</li></settlement></list><tree><country name="Allemagne"><noRegion><name sortKey="Holscher, Christoph" sort="Holscher, Christoph" uniqKey="Holscher C" first="Christoph" last="Hölscher">Christoph Hölscher</name></noRegion><name sortKey="Ehlers, Stefan" sort="Ehlers, Stefan" uniqKey="Ehlers S" first="Stefan" last="Ehlers">Stefan Ehlers</name><name sortKey="Heitmann, Lisa" sort="Heitmann, Lisa" uniqKey="Heitmann L" first="Lisa" last="Heitmann">Lisa Heitmann</name><name sortKey="Horstmann, Rolf D" sort="Horstmann, Rolf D" uniqKey="Horstmann R" first="Rolf D" last="Horstmann">Rolf D. Horstmann</name><name sortKey="Meyer, Christian G" sort="Meyer, Christian G" uniqKey="Meyer C" first="Christian G" last="Meyer">Christian G. Meyer</name><name sortKey="Thye, Thorsten" sort="Thye, Thorsten" uniqKey="Thye T" first="Thorsten" last="Thye">Thorsten Thye</name></country><country name="Ghana"><noRegion><name sortKey="Owusu Dabo, Ellis" sort="Owusu Dabo, Ellis" uniqKey="Owusu Dabo E" first="Ellis" last="Owusu-Dabo">Ellis Owusu-Dabo</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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