IL-22Ra1 is induced during influenza infection by direct and indirect TLR3 induction of STAT1.
Identifieur interne : 000049 ( PubMed/Checkpoint ); précédent : 000048; suivant : 000050IL-22Ra1 is induced during influenza infection by direct and indirect TLR3 induction of STAT1.
Auteurs : K D Hebert [États-Unis] ; N. Mclaughlin [États-Unis] ; Zhe Zhang [États-Unis] ; A. Cipriani [États-Unis] ; J F Alcorn [États-Unis] ; D A Pociask [États-Unis]Source :
- Respiratory research [ 1465-993X ] ; 2019.
Descripteurs français
- KwdFr :
- Animaux, Cellules A549, Chloroquine (pharmacologie), Facteur de transcription STAT-1 (biosynthèse), Grippe humaine (anatomopathologie), Grippe humaine (métabolisme), Humains, Interférons (pharmacologie), Mâle, Poly I-C (pharmacologie), Récepteur de type Toll-3 (biosynthèse), Récepteurs aux interleukines (biosynthèse), Souris, Souris de lignée C57BL.
- MESH :
- anatomopathologie : Grippe humaine.
- biosynthèse : Facteur de transcription STAT-1, Récepteur de type Toll-3, Récepteurs aux interleukines.
- métabolisme : Grippe humaine.
- pharmacologie : Chloroquine, Interférons, Poly I-C.
- Animaux, Cellules A549, Humains, Mâle, Souris, Souris de lignée C57BL.
English descriptors
- KwdEn :
- A549 Cells, Animals, Chloroquine (pharmacology), Humans, Influenza, Human (metabolism), Influenza, Human (pathology), Interferons (pharmacology), Male, Mice, Mice, Inbred C57BL, Poly I-C (pharmacology), Receptors, Interleukin (biosynthesis), STAT1 Transcription Factor (biosynthesis), Toll-Like Receptor 3 (biosynthesis).
- MESH :
- chemical , biosynthesis : Receptors, Interleukin, STAT1 Transcription Factor, Toll-Like Receptor 3.
- chemical , pharmacology : Chloroquine, Interferons, Poly I-C.
- metabolism : Influenza, Human.
- pathology : Influenza, Human.
- A549 Cells, Animals, Humans, Male, Mice, Mice, Inbred C57BL.
Abstract
Influenza attacks the epithelium of the lung, causing cell death and disruption of the epithelial barrier leading to fluid buildup in the lung and impairment of gas exchange. Limited treatment options for severe influenza pneumonia prioritize the need for the discovery of effective therapies. IL-22 is a cytokine that promotes tissue integrity and has strong promise as a treatment option. While research has been focused on the cytokine itself, there is limited understanding of the regulation of the IL-22 receptor (IL-22Ra1) at the epithelial surface during infection.
DOI: 10.1186/s12931-019-1153-4
PubMed: 31416461
Affiliations:
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Mclaughlin</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medicine, Pulmonary Diseases, Critical Care & Environmental Medicine, Tulane University School of Medicine, 1430 Tulane Ave. Mail code sl279, New Orleans, LA, 70112, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Pulmonary Diseases, Critical Care & Environmental Medicine, Tulane University School of Medicine, 1430 Tulane Ave. Mail code sl279, New Orleans, LA, 70112</wicri:regionArea><wicri:noRegion>70112</wicri:noRegion></affiliation></author><author><name sortKey="Zhang, Zhe" sort="Zhang, Zhe" uniqKey="Zhang Z" first="Zhe" last="Zhang">Zhe Zhang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medicine, Pulmonary Diseases, Critical Care & Environmental Medicine, Tulane University School of Medicine, 1430 Tulane Ave. Mail code sl279, New Orleans, LA, 70112, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Pulmonary Diseases, Critical Care & Environmental Medicine, Tulane University School of Medicine, 1430 Tulane Ave. Mail code sl279, New Orleans, LA, 70112</wicri:regionArea><wicri:noRegion>70112</wicri:noRegion></affiliation></author><author><name sortKey="Cipriani, A" sort="Cipriani, A" uniqKey="Cipriani A" first="A" last="Cipriani">A. Cipriani</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pediatrics, Children's Hospital of Pittsburgh of UPMC, One Children's Hospital Drive, 4401 Penn Ave, Pittsburgh, PA, 15224, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pediatrics, Children's Hospital of Pittsburgh of UPMC, One Children's Hospital Drive, 4401 Penn Ave, Pittsburgh, PA, 15224</wicri:regionArea><wicri:noRegion>15224</wicri:noRegion></affiliation></author><author><name sortKey="Alcorn, J F" sort="Alcorn, J F" uniqKey="Alcorn J" first="J F" last="Alcorn">J F Alcorn</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pediatrics, Children's Hospital of Pittsburgh of UPMC, One Children's Hospital Drive, 4401 Penn Ave, Pittsburgh, PA, 15224, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pediatrics, Children's Hospital of Pittsburgh of UPMC, One Children's Hospital Drive, 4401 Penn Ave, Pittsburgh, PA, 15224</wicri:regionArea><wicri:noRegion>15224</wicri:noRegion></affiliation></author><author><name sortKey="Pociask, D A" sort="Pociask, D A" uniqKey="Pociask D" first="D A" last="Pociask">D A Pociask</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medicine, Pulmonary Diseases, Critical Care & Environmental Medicine, Tulane University School of Medicine, 1430 Tulane Ave. Mail code sl279, New Orleans, LA, 70112, USA. dpociask@tulane.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Pulmonary Diseases, Critical Care & Environmental Medicine, Tulane University School of Medicine, 1430 Tulane Ave. Mail code sl279, New Orleans, LA, 70112</wicri:regionArea><wicri:noRegion>70112</wicri:noRegion></affiliation></author></analytic><series><title level="j">Respiratory research</title><idno type="eISSN">1465-993X</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>A549 Cells</term><term>Animals</term><term>Chloroquine (pharmacology)</term><term>Humans</term><term>Influenza, Human (metabolism)</term><term>Influenza, Human (pathology)</term><term>Interferons (pharmacology)</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Poly I-C (pharmacology)</term><term>Receptors, Interleukin (biosynthesis)</term><term>STAT1 Transcription Factor (biosynthesis)</term><term>Toll-Like Receptor 3 (biosynthesis)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Cellules A549</term><term>Chloroquine (pharmacologie)</term><term>Facteur de transcription STAT-1 (biosynthèse)</term><term>Grippe humaine (anatomopathologie)</term><term>Grippe humaine (métabolisme)</term><term>Humains</term><term>Interférons (pharmacologie)</term><term>Mâle</term><term>Poly I-C (pharmacologie)</term><term>Récepteur de type Toll-3 (biosynthèse)</term><term>Récepteurs aux interleukines (biosynthèse)</term><term>Souris</term><term>Souris de lignée C57BL</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Receptors, Interleukin</term><term>STAT1 Transcription Factor</term><term>Toll-Like Receptor 3</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Chloroquine</term><term>Interferons</term><term>Poly I-C</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Grippe humaine</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Facteur de transcription STAT-1</term><term>Récepteur de type Toll-3</term><term>Récepteurs aux interleukines</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Influenza, Human</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Grippe humaine</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Influenza, Human</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Chloroquine</term><term>Interférons</term><term>Poly I-C</term></keywords><keywords scheme="MESH" xml:lang="en"><term>A549 Cells</term><term>Animals</term><term>Humans</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules A549</term><term>Humains</term><term>Mâle</term><term>Souris</term><term>Souris de lignée C57BL</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Influenza attacks the epithelium of the lung, causing cell death and disruption of the epithelial barrier leading to fluid buildup in the lung and impairment of gas exchange. Limited treatment options for severe influenza pneumonia prioritize the need for the discovery of effective therapies. IL-22 is a cytokine that promotes tissue integrity and has strong promise as a treatment option. While research has been focused on the cytokine itself, there is limited understanding of the regulation of the IL-22 receptor (IL-22Ra1) at the epithelial surface during infection.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31416461</PMID><DateCompleted><Year>2020</Year><Month>02</Month><Day>03</Day></DateCompleted><DateRevised><Year>2020</Year><Month>02</Month><Day>25</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1465-993X</ISSN><JournalIssue CitedMedium="Internet"><Volume>20</Volume><Issue>1</Issue><PubDate><Year>2019</Year><Month>Aug</Month><Day>15</Day></PubDate></JournalIssue><Title>Respiratory research</Title><ISOAbbreviation>Respir. Res.</ISOAbbreviation></Journal><ArticleTitle>IL-22Ra1 is induced during influenza infection by direct and indirect TLR3 induction of STAT1.</ArticleTitle><Pagination><MedlinePgn>184</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1186/s12931-019-1153-4</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Influenza attacks the epithelium of the lung, causing cell death and disruption of the epithelial barrier leading to fluid buildup in the lung and impairment of gas exchange. Limited treatment options for severe influenza pneumonia prioritize the need for the discovery of effective therapies. IL-22 is a cytokine that promotes tissue integrity and has strong promise as a treatment option. While research has been focused on the cytokine itself, there is limited understanding of the regulation of the IL-22 receptor (IL-22Ra1) at the epithelial surface during infection.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">IL-22Ra1 levels were measured by qRT-PCR, western blot and immunofluorescence following H1N1 influenza infection (A/PR/8/34 H1N1) or synthetic TLR3 mimetic, Poly (I:C). Regulation of the receptor was determined using STAT inhibitors (STAT1, STAT3 and PanSTAT inhibitors), TLR3 inhibition, and neutralization of interferon alpha receptor 2 (IFNAR2). Significance was determined by a p-value of greater than 0.05. Significance between two groups was measured using unpaired t-test and significance between more than two groups was measured using one-way ANOVA with Tukey Multiple Comparison Test.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Here we show both in vivo and in vitro that IL-22Ra1 was induced as early as 24 h after influenza (H1N1 PR8) infection. This induction was triggered by toll-like receptor 3 (TLR3) as a TLR3 mimetic [Poly (I:C)] also induced IL-22Ra1 and inhibition of endosomal formation required for TLR3 function inhibited this process. This upregulation was dependent upon IFNβ signaling through STAT1. Importantly, induction of IL-22Ra1 significantly increased IL-22 signaling as evidenced by pSTAT3 levels following IL-22 treatment.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Collectively, these data suggest epithelial cells may optimize the beneficial effects of IL-22 through the induction of the IL-22 receptor during viral infection in the lung.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hebert</LastName><ForeName>K D</ForeName><Initials>KD</Initials><AffiliationInfo><Affiliation>Department of Medicine, Pulmonary Diseases, Critical Care & Environmental Medicine, Tulane University School of Medicine, 1430 Tulane Ave. Mail code sl279, New Orleans, LA, 70112, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mclaughlin</LastName><ForeName>N</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Medicine, Pulmonary Diseases, Critical Care & Environmental Medicine, Tulane University School of Medicine, 1430 Tulane Ave. Mail code sl279, New Orleans, LA, 70112, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Zhe</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Medicine, Pulmonary Diseases, Critical Care & Environmental Medicine, Tulane University School of Medicine, 1430 Tulane Ave. Mail code sl279, New Orleans, LA, 70112, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cipriani</LastName><ForeName>A</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, Children's Hospital of Pittsburgh of UPMC, One Children's Hospital Drive, 4401 Penn Ave, Pittsburgh, PA, 15224, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alcorn</LastName><ForeName>J F</ForeName><Initials>JF</Initials><AffiliationInfo><Affiliation>Department of Pediatrics, Children's Hospital of Pittsburgh of UPMC, One Children's Hospital Drive, 4401 Penn Ave, Pittsburgh, PA, 15224, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pociask</LastName><ForeName>D A</ForeName><Initials>DA</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-1256-6410</Identifier><AffiliationInfo><Affiliation>Department of Medicine, Pulmonary Diseases, Critical Care & Environmental Medicine, Tulane University School of Medicine, 1430 Tulane Ave. Mail code sl279, New Orleans, LA, 70112, USA. dpociask@tulane.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 HL107380</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>1R21AI117569</GrantID><Agency>National Institute of Allergy and Infectious Diseases</Agency><Country></Country></Grant><Grant><GrantID>1R01HL122760</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>08</Month><Day>15</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Respir Res</MedlineTA><NlmUniqueID>101090633</NlmUniqueID><ISSNLinking>1465-9921</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018123">Receptors, Interleukin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050794">STAT1 Transcription Factor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C494079">STAT1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C495344">TLR3 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051196">Toll-Like Receptor 3</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C415369">interleukin-22 receptor</NameOfSubstance></Chemical><Chemical><RegistryNumber>886U3H6UFF</RegistryNumber><NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance></Chemical><Chemical><RegistryNumber>9008-11-1</RegistryNumber><NameOfSubstance UI="D007372">Interferons</NameOfSubstance></Chemical><Chemical><RegistryNumber>O84C90HH2L</RegistryNumber><NameOfSubstance UI="D011070">Poly I-C</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000072283" MajorTopicYN="N">A549 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002738" MajorTopicYN="N">Chloroquine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007251" MajorTopicYN="N">Influenza, Human</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007372" MajorTopicYN="N">Interferons</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011070" MajorTopicYN="N">Poly I-C</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018123" MajorTopicYN="N">Receptors, Interleukin</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050794" MajorTopicYN="N">STAT1 Transcription Factor</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051196" MajorTopicYN="N">Toll-Like Receptor 3</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">IFNβ</Keyword><Keyword MajorTopicYN="N">IL-22</Keyword><Keyword MajorTopicYN="N">IL-22Ra1</Keyword><Keyword MajorTopicYN="N">Influenza</Keyword><Keyword MajorTopicYN="N">STAT1</Keyword><Keyword MajorTopicYN="N">TLR3</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate 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