HIF-1α regulates IL-1β and IL-17 in sarcoidosis.
Identifieur interne : 000057 ( PubMed/Corpus ); précédent : 000056; suivant : 000058HIF-1α regulates IL-1β and IL-17 in sarcoidosis.
Auteurs : Jaya Talreja ; Harvinder Talwar ; Christian Bauerfeld ; Lawrence I. Grossman ; Kezhong Zhang ; Paul Tranchida ; Lobelia SamavatiSource :
- eLife [ 2050-084X ] ; 2019.
English descriptors
- KwdEn :
- Adolescent, Adult, Female, Gene Expression Regulation, Humans, Hypoxia-Inducible Factor 1, alpha Subunit (metabolism), Inflammation (pathology), Interleukin-17 (biosynthesis), Interleukin-1beta (biosynthesis), Lung (pathology), Macrophages (pathology), Male, Monocytes (pathology), Sarcoidosis (pathology), Th1 Cells (immunology), Th17 Cells (immunology), Young Adult.
- MESH :
- chemical , biosynthesis : Interleukin-17, Interleukin-1beta.
- chemical , metabolism : Hypoxia-Inducible Factor 1, alpha Subunit.
- immunology : Th1 Cells, Th17 Cells.
- pathology : Inflammation, Lung, Macrophages, Monocytes, Sarcoidosis.
- Adolescent, Adult, Female, Gene Expression Regulation, Humans, Male, Young Adult.
Abstract
Sarcoidosis is a complex systemic granulomatous disease of unknown etiology characterized by the presence of activated macrophages and Th1/Th17 effector cells. Data mining of our RNA-Seq analysis of CD14+monocytes showed enrichment for metabolic and hypoxia inducible factor (HIF) pathways in sarcoidosis. Further investigation revealed that sarcoidosis macrophages and monocytes exhibit higher protein levels for HIF-α isoforms, HIF-1β, and their transcriptional co-activator p300 as well as glucose transporter 1 (Glut1). In situ hybridization of sarcoidosis granulomatous lung tissues showed abundance of HIF-1α in the center of granulomas. The abundance of HIF isoforms was mechanistically linked to elevated IL-1β and IL-17 since targeted down regulation of HIF-1α via short interfering RNA or a HIF-1α inhibitor decreased their production. Pharmacological intervention using chloroquine, a lysosomal inhibitor, decreased lysosomal associated protein 2 (LAMP2) and HIF-1α levels and modified cytokine production. These data suggest that increased activity of HIF-α isoforms regulate Th1/Th17 mediated inflammation in sarcoidosis.
DOI: 10.7554/eLife.44519
PubMed: 30946009
Links to Exploration step
pubmed:30946009Le document en format XML
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Grossman</name><affiliation><nlm:affiliation>Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, United States.</nlm:affiliation></affiliation></author><author><name sortKey="Zhang, Kezhong" sort="Zhang, Kezhong" uniqKey="Zhang K" first="Kezhong" last="Zhang">Kezhong Zhang</name><affiliation><nlm:affiliation>Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, United States.</nlm:affiliation></affiliation></author><author><name sortKey="Tranchida, Paul" sort="Tranchida, Paul" uniqKey="Tranchida P" first="Paul" last="Tranchida">Paul Tranchida</name><affiliation><nlm:affiliation>Department of Pathology, Wayne State University School of Medicine and Detroit Medical Center, Detroit, United States.</nlm:affiliation></affiliation></author><author><name sortKey="Samavati, Lobelia" sort="Samavati, Lobelia" uniqKey="Samavati L" first="Lobelia" last="Samavati">Lobelia Samavati</name><affiliation><nlm:affiliation>Department of Internal Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Wayne State University School of Medicine and Detroit Medical Center, Detroit, United States.</nlm:affiliation></affiliation></author></analytic><series><title level="j">eLife</title><idno type="eISSN">2050-084X</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Female</term><term>Gene Expression Regulation</term><term>Humans</term><term>Hypoxia-Inducible Factor 1, alpha Subunit (metabolism)</term><term>Inflammation (pathology)</term><term>Interleukin-17 (biosynthesis)</term><term>Interleukin-1beta (biosynthesis)</term><term>Lung (pathology)</term><term>Macrophages (pathology)</term><term>Male</term><term>Monocytes (pathology)</term><term>Sarcoidosis (pathology)</term><term>Th1 Cells (immunology)</term><term>Th17 Cells (immunology)</term><term>Young Adult</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Interleukin-17</term><term>Interleukin-1beta</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Hypoxia-Inducible Factor 1, alpha Subunit</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Th1 Cells</term><term>Th17 Cells</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Inflammation</term><term>Lung</term><term>Macrophages</term><term>Monocytes</term><term>Sarcoidosis</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Female</term><term>Gene Expression Regulation</term><term>Humans</term><term>Male</term><term>Young Adult</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Sarcoidosis is a complex systemic granulomatous disease of unknown etiology characterized by the presence of activated macrophages and Th1/Th17 effector cells. Data mining of our RNA-Seq analysis of CD14<sup>+</sup>monocytes showed enrichment for metabolic and hypoxia inducible factor (HIF) pathways in sarcoidosis. Further investigation revealed that sarcoidosis macrophages and monocytes exhibit higher protein levels for HIF-α isoforms, HIF-1β, and their transcriptional co-activator p300 as well as glucose transporter 1 (Glut1). In situ hybridization of sarcoidosis granulomatous lung tissues showed abundance of HIF-1α in the center of granulomas. The abundance of HIF isoforms was mechanistically linked to elevated IL-1β and IL-17 since targeted down regulation of HIF-1α via short interfering RNA or a HIF-1α inhibitor decreased their production. Pharmacological intervention using chloroquine, a lysosomal inhibitor, decreased lysosomal associated protein 2 (LAMP2) and HIF-1α levels and modified cytokine production. These data suggest that increased activity of HIF-α isoforms regulate Th1/Th17 mediated inflammation in sarcoidosis.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30946009</PMID><DateCompleted><Year>2020</Year><Month>03</Month><Day>11</Day></DateCompleted><DateRevised><Year>2020</Year><Month>03</Month><Day>20</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2050-084X</ISSN><JournalIssue CitedMedium="Internet"><Volume>8</Volume><PubDate><Year>2019</Year><Month>05</Month><Day>01</Day></PubDate></JournalIssue><Title>eLife</Title><ISOAbbreviation>Elife</ISOAbbreviation></Journal><ArticleTitle>HIF-1α regulates IL-1β and IL-17 in sarcoidosis.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.7554/eLife.44519</ELocationID><ELocationID EIdType="pii" ValidYN="Y">e44519</ELocationID><Abstract><AbstractText>Sarcoidosis is a complex systemic granulomatous disease of unknown etiology characterized by the presence of activated macrophages and Th1/Th17 effector cells. Data mining of our RNA-Seq analysis of CD14<sup>+</sup>monocytes showed enrichment for metabolic and hypoxia inducible factor (HIF) pathways in sarcoidosis. Further investigation revealed that sarcoidosis macrophages and monocytes exhibit higher protein levels for HIF-α isoforms, HIF-1β, and their transcriptional co-activator p300 as well as glucose transporter 1 (Glut1). In situ hybridization of sarcoidosis granulomatous lung tissues showed abundance of HIF-1α in the center of granulomas. The abundance of HIF isoforms was mechanistically linked to elevated IL-1β and IL-17 since targeted down regulation of HIF-1α via short interfering RNA or a HIF-1α inhibitor decreased their production. Pharmacological intervention using chloroquine, a lysosomal inhibitor, decreased lysosomal associated protein 2 (LAMP2) and HIF-1α levels and modified cytokine production. These data suggest that increased activity of HIF-α isoforms regulate Th1/Th17 mediated inflammation in sarcoidosis.</AbstractText><CopyrightInformation>© 2019, Talreja et al.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Talreja</LastName><ForeName>Jaya</ForeName><Initials>J</Initials><Identifier Source="ORCID">0000-0001-6557-6500</Identifier><AffiliationInfo><Affiliation>Department of Internal Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Wayne State University School of Medicine and Detroit Medical Center, Detroit, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Talwar</LastName><ForeName>Harvinder</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Wayne State University School of Medicine and Detroit Medical Center, Detroit, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bauerfeld</LastName><ForeName>Christian</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, Division of Critical Care, Wayne State University School of Medicine and Detroit Medical Center, Detroit, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Grossman</LastName><ForeName>Lawrence I</ForeName><Initials>LI</Initials><AffiliationInfo><Affiliation>Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Kezhong</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tranchida</LastName><ForeName>Paul</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Pathology, Wayne State University School of Medicine and Detroit Medical Center, Detroit, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Samavati</LastName><ForeName>Lobelia</ForeName><Initials>L</Initials><Identifier Source="ORCID">0000-0002-3327-2585</Identifier><AffiliationInfo><Affiliation>Department of Internal Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Wayne State University School of Medicine and Detroit Medical Center, Detroit, United States.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>W81XWH-16-1-0516</GrantID><Agency>U.S. Department of Defense</Agency><Country>International</Country></Grant><Grant><GrantID>R01 HL113508</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01HL113508</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 DK090313</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 CA022453</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>Henry L Brasza endowment</GrantID><Agency>Wayne State University</Agency><Country>International</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>05</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Elife</MedlineTA><NlmUniqueID>101579614</NlmUniqueID><ISSNLinking>2050-084X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C497442">HIF1A protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051795">Hypoxia-Inducible Factor 1, alpha Subunit</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020381">Interleukin-17</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053583">Interleukin-1beta</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000293" MajorTopicYN="N">Adolescent</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="Y">Gene Expression Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051795" MajorTopicYN="N">Hypoxia-Inducible Factor 1, alpha Subunit</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020381" MajorTopicYN="N">Interleukin-17</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053583" MajorTopicYN="N">Interleukin-1beta</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009000" MajorTopicYN="N">Monocytes</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012507" MajorTopicYN="N">Sarcoidosis</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018417" MajorTopicYN="N">Th1 Cells</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058504" MajorTopicYN="N">Th17 Cells</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055815" MajorTopicYN="N">Young Adult</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">HIF-1α</Keyword><Keyword MajorTopicYN="Y">IL-17</Keyword><Keyword MajorTopicYN="Y">IL-1β</Keyword><Keyword MajorTopicYN="Y">alveolar macrophages</Keyword><Keyword MajorTopicYN="Y">human biology</Keyword><Keyword MajorTopicYN="Y">immunology</Keyword><Keyword MajorTopicYN="Y">inflammation</Keyword><Keyword MajorTopicYN="Y">medicine</Keyword><Keyword MajorTopicYN="Y">monocytes</Keyword><Keyword MajorTopicYN="Y">none</Keyword><Keyword MajorTopicYN="Y">sarcoidosis</Keyword></KeywordList><CoiStatement>JT, HT, CB, LG, KZ, PT, LS No competing 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