Glutathione Fine-Tunes the Innate Immune Response toward Antiviral Pathways in a Macrophage Cell Line Independently of Its Antioxidant Properties.
Identifieur interne : 000327 ( PubMed/Checkpoint ); précédent : 000326; suivant : 000328Glutathione Fine-Tunes the Innate Immune Response toward Antiviral Pathways in a Macrophage Cell Line Independently of Its Antioxidant Properties.
Auteurs : Marina Diotallevi [Royaume-Uni] ; Paola Checconi [Italie] ; Anna Teresa Palamara [Italie] ; Ignacio Celestino [Italie] ; Lucia Coppo [Suède] ; Arne Holmgren [Suède] ; Kahina Abbas [France] ; Fabienne Peyrot [France] ; Manuela Mengozzi [Royaume-Uni] ; Pietro Ghezzi [Royaume-Uni]Source :
- Frontiers in immunology [ 1664-3224 ] ; 2017.
Abstract
Glutathione (GSH), a major cellular antioxidant, is considered an inhibitor of the inflammatory response involving reactive oxygen species (ROS). However, evidence is largely based on experiments with exogenously added antioxidants/reducing agents or pro-oxidants. We show that depleting macrophages of 99% of GSH does not exacerbate the inflammatory gene expression profile in the RAW264 macrophage cell line or increase expression of inflammatory cytokines in response to the toll-like receptor 4 (TLR4) agonist lipopolysaccharide (LPS); only two small patterns of LPS-induced genes were sensitive to GSH depletion. One group, mapping to innate immunity and antiviral responses (Oas2, Oas3, Mx2, Irf7, Irf9, STAT1, il1b), required GSH for optimal induction. Consequently, GSH depletion prevented the LPS-induced activation of antiviral response and its inhibition of influenza virus infection. LPS induction of a second group of genes (Prdx1, Srxn1, Hmox1, GSH synthase, cysteine transporters), mapping to nrf2 and the oxidative stress response, was increased by GSH depletion. We conclude that the main function of endogenous GSH is not to limit inflammation but to fine-tune the innate immune response to infection.
DOI: 10.3389/fimmu.2017.01239
PubMed: 29033950
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sortKey="Diotallevi, Marina" sort="Diotallevi, Marina" uniqKey="Diotallevi M" first="Marina" last="Diotallevi">Marina Diotallevi</name><affiliation wicri:level="1"><nlm:affiliation>Brighton and Sussex Medical School, Brighton, United Kingdom.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Brighton and Sussex Medical School, Brighton</wicri:regionArea><wicri:noRegion>Brighton</wicri:noRegion></affiliation></author><author><name sortKey="Checconi, Paola" sort="Checconi, Paola" uniqKey="Checconi P" first="Paola" last="Checconi">Paola Checconi</name><affiliation wicri:level="3"><nlm:affiliation>Department of Public Health and Infectious Diseases, Sapienza University of Rome, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Rome, Italy.</nlm:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Public Health and Infectious Diseases, Sapienza University of Rome, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Rome</wicri:regionArea><placeName><settlement type="city">Rome</settlement><region nuts="2">Latium</region></placeName></affiliation></author><author><name sortKey="Palamara, Anna Teresa" sort="Palamara, Anna Teresa" uniqKey="Palamara A" first="Anna Teresa" last="Palamara">Anna Teresa Palamara</name><affiliation wicri:level="3"><nlm:affiliation>Department of Public Health and Infectious Diseases, Sapienza University of Rome, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Rome, Italy.</nlm:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Public Health and Infectious Diseases, Sapienza University of Rome, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Rome</wicri:regionArea><placeName><settlement type="city">Rome</settlement><region nuts="2">Latium</region></placeName></affiliation></author><author><name sortKey="Celestino, Ignacio" sort="Celestino, Ignacio" uniqKey="Celestino I" first="Ignacio" last="Celestino">Ignacio Celestino</name><affiliation wicri:level="3"><nlm:affiliation>IRCCS, San Raffaele Pisana, Telematic University, Rome, Italy.</nlm:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>IRCCS, San Raffaele Pisana, Telematic University, Rome</wicri:regionArea><placeName><settlement type="city">Rome</settlement><region nuts="2">Latium</region></placeName></affiliation></author><author><name sortKey="Coppo, Lucia" sort="Coppo, Lucia" uniqKey="Coppo L" first="Lucia" last="Coppo">Lucia Coppo</name><affiliation wicri:level="3"><nlm:affiliation>Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm</wicri:regionArea><placeName><settlement type="city">Stockholm</settlement><region nuts="2">Svealand</region></placeName></affiliation></author><author><name sortKey="Holmgren, Arne" sort="Holmgren, Arne" uniqKey="Holmgren A" first="Arne" last="Holmgren">Arne Holmgren</name><affiliation wicri:level="3"><nlm:affiliation>Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm</wicri:regionArea><placeName><settlement type="city">Stockholm</settlement><region nuts="2">Svealand</region></placeName></affiliation></author><author><name sortKey="Abbas, Kahina" sort="Abbas, Kahina" uniqKey="Abbas K" first="Kahina" last="Abbas">Kahina Abbas</name><affiliation wicri:level="3"><nlm:affiliation>LCBPT, UMR 8601 CNRS-Paris Descartes University, Sorbonne Paris Cité, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>LCBPT, UMR 8601 CNRS-Paris Descartes University, Sorbonne Paris Cité, Paris</wicri:regionArea><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Peyrot, Fabienne" sort="Peyrot, Fabienne" uniqKey="Peyrot F" first="Fabienne" last="Peyrot">Fabienne Peyrot</name><affiliation wicri:level="3"><nlm:affiliation>LCBPT, UMR 8601 CNRS-Paris Descartes University, Sorbonne Paris Cité, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>LCBPT, UMR 8601 CNRS-Paris Descartes University, Sorbonne Paris Cité, Paris</wicri:regionArea><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Mengozzi, Manuela" sort="Mengozzi, Manuela" uniqKey="Mengozzi M" first="Manuela" last="Mengozzi">Manuela Mengozzi</name><affiliation wicri:level="1"><nlm:affiliation>Brighton and Sussex Medical School, Brighton, United Kingdom.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Brighton and Sussex Medical School, Brighton</wicri:regionArea><wicri:noRegion>Brighton</wicri:noRegion></affiliation></author><author><name sortKey="Ghezzi, Pietro" sort="Ghezzi, Pietro" uniqKey="Ghezzi P" first="Pietro" last="Ghezzi">Pietro Ghezzi</name><affiliation wicri:level="1"><nlm:affiliation>Brighton and Sussex Medical School, Brighton, United Kingdom.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Brighton and Sussex Medical School, Brighton</wicri:regionArea><wicri:noRegion>Brighton</wicri:noRegion></affiliation></author></analytic><series><title level="j">Frontiers in immunology</title><idno type="ISSN">1664-3224</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Glutathione (GSH), a major cellular antioxidant, is considered an inhibitor of the inflammatory response involving reactive oxygen species (ROS). However, evidence is largely based on experiments with exogenously added antioxidants/reducing agents or pro-oxidants. We show that depleting macrophages of 99% of GSH does not exacerbate the inflammatory gene expression profile in the RAW264 macrophage cell line or increase expression of inflammatory cytokines in response to the toll-like receptor 4 (TLR4) agonist lipopolysaccharide (LPS); only two small patterns of LPS-induced genes were sensitive to GSH depletion. One group, mapping to innate immunity and antiviral responses (Oas2, Oas3, Mx2, Irf7, Irf9, STAT1, il1b), required GSH for optimal induction. Consequently, GSH depletion prevented the LPS-induced activation of antiviral response and its inhibition of influenza virus infection. LPS induction of a second group of genes (Prdx1, Srxn1, Hmox1, GSH synthase, cysteine transporters), mapping to nrf2 and the oxidative stress response, was increased by GSH depletion. We conclude that the main function of endogenous GSH is not to limit inflammation but to fine-tune the innate immune response to infection.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">29033950</PMID><DateRevised><Year>2019</Year><Month>11</Month><Day>20</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Print">1664-3224</ISSN><JournalIssue CitedMedium="Print"><Volume>8</Volume><PubDate><Year>2017</Year></PubDate></JournalIssue><Title>Frontiers in immunology</Title><ISOAbbreviation>Front Immunol</ISOAbbreviation></Journal><ArticleTitle>Glutathione Fine-Tunes the Innate Immune Response toward Antiviral Pathways in a Macrophage Cell Line Independently of Its Antioxidant Properties.</ArticleTitle><Pagination><MedlinePgn>1239</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3389/fimmu.2017.01239</ELocationID><Abstract><AbstractText>Glutathione (GSH), a major cellular antioxidant, is considered an inhibitor of the inflammatory response involving reactive oxygen species (ROS). However, evidence is largely based on experiments with exogenously added antioxidants/reducing agents or pro-oxidants. We show that depleting macrophages of 99% of GSH does not exacerbate the inflammatory gene expression profile in the RAW264 macrophage cell line or increase expression of inflammatory cytokines in response to the toll-like receptor 4 (TLR4) agonist lipopolysaccharide (LPS); only two small patterns of LPS-induced genes were sensitive to GSH depletion. One group, mapping to innate immunity and antiviral responses (Oas2, Oas3, Mx2, Irf7, Irf9, STAT1, il1b), required GSH for optimal induction. Consequently, GSH depletion prevented the LPS-induced activation of antiviral response and its inhibition of influenza virus infection. LPS induction of a second group of genes (Prdx1, Srxn1, Hmox1, GSH synthase, cysteine transporters), mapping to nrf2 and the oxidative stress response, was increased by GSH depletion. We conclude that the main function of endogenous GSH is not to limit inflammation but to fine-tune the innate immune response to infection.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Diotallevi</LastName><ForeName>Marina</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Brighton and Sussex Medical School, Brighton, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Checconi</LastName><ForeName>Paola</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Public Health and Infectious Diseases, Sapienza University of Rome, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Palamara</LastName><ForeName>Anna Teresa</ForeName><Initials>AT</Initials><AffiliationInfo><Affiliation>Department of Public Health and Infectious Diseases, Sapienza University of Rome, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Rome, Italy.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>IRCCS, San Raffaele Pisana, Telematic University, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Celestino</LastName><ForeName>Ignacio</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>IRCCS, San Raffaele Pisana, Telematic University, Rome, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Coppo</LastName><ForeName>Lucia</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Holmgren</LastName><ForeName>Arne</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Abbas</LastName><ForeName>Kahina</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>LCBPT, UMR 8601 CNRS-Paris Descartes University, Sorbonne Paris Cité, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Peyrot</LastName><ForeName>Fabienne</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>LCBPT, UMR 8601 CNRS-Paris Descartes University, Sorbonne Paris Cité, Paris, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>ESPE of Paris, Paris Sorbonne University, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mengozzi</LastName><ForeName>Manuela</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Brighton and Sussex Medical School, Brighton, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ghezzi</LastName><ForeName>Pietro</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Brighton and Sussex Medical School, Brighton, United Kingdom.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>09</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Front Immunol</MedlineTA><NlmUniqueID>101560960</NlmUniqueID><ISSNLinking>1664-3224</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">TLR4</Keyword><Keyword MajorTopicYN="N">antiviral immunity</Keyword><Keyword MajorTopicYN="N">glutathione</Keyword><Keyword MajorTopicYN="N">inflammation</Keyword><Keyword MajorTopicYN="N">influenza</Keyword><Keyword MajorTopicYN="N">innate immunity</Keyword><Keyword MajorTopicYN="N">macrophages</Keyword><Keyword MajorTopicYN="N">redox regulation</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate 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name="Italie"><region name="Latium"><name sortKey="Checconi, Paola" sort="Checconi, Paola" uniqKey="Checconi P" first="Paola" last="Checconi">Paola Checconi</name></region><name sortKey="Celestino, Ignacio" sort="Celestino, Ignacio" uniqKey="Celestino I" first="Ignacio" last="Celestino">Ignacio Celestino</name><name sortKey="Palamara, Anna Teresa" sort="Palamara, Anna Teresa" uniqKey="Palamara A" first="Anna Teresa" last="Palamara">Anna Teresa Palamara</name></country><country name="Suède"><region name="Svealand"><name sortKey="Coppo, Lucia" sort="Coppo, Lucia" uniqKey="Coppo L" first="Lucia" last="Coppo">Lucia Coppo</name></region><name sortKey="Holmgren, Arne" sort="Holmgren, Arne" uniqKey="Holmgren A" first="Arne" last="Holmgren">Arne Holmgren</name></country><country name="France"><region name="Île-de-France"><name sortKey="Abbas, Kahina" sort="Abbas, Kahina" uniqKey="Abbas K" first="Kahina" last="Abbas">Kahina Abbas</name></region><name sortKey="Peyrot, Fabienne" sort="Peyrot, Fabienne" uniqKey="Peyrot F" first="Fabienne" last="Peyrot">Fabienne Peyrot</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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