Macrophage interleukin-6 and tumour necrosis factor-alpha are induced by coronavirus fixation to Toll-like receptor 2/heparan sulphate receptors but not carcinoembryonic cell adhesion antigen 1a.
Identifieur interne : 001823 ( PubMed/Corpus ); précédent : 001822; suivant : 001824Macrophage interleukin-6 and tumour necrosis factor-alpha are induced by coronavirus fixation to Toll-like receptor 2/heparan sulphate receptors but not carcinoembryonic cell adhesion antigen 1a.
Auteurs : Alexandre Jacques ; Christian Bleau ; Claire Turbide ; Nicole Beauchemin ; Lucie LamontagneSource :
- Immunology [ 1365-2567 ] ; 2009.
English descriptors
- KwdEn :
- Animals, Butadienes (pharmacology), Carcinoembryonic Antigen (genetics), Carcinoembryonic Antigen (metabolism), Cell Line, Coronavirus Infections (complications), Enzyme Inhibitors (pharmacology), Fibroblasts (drug effects), Fibroblasts (metabolism), Fibroblasts (virology), Heparitin Sulfate (immunology), Heparitin Sulfate (metabolism), Hepatitis, Animal (immunology), Hepatitis, Animal (virology), Imidazoles (pharmacology), Interleukin-6 (agonists), Interleukin-6 (biosynthesis), Liver (immunology), Liver (pathology), Liver (virology), Macrophages, Peritoneal (drug effects), Macrophages, Peritoneal (immunology), Macrophages, Peritoneal (virology), Membrane Glycoproteins (immunology), Mice, Mice, Knockout, Murine hepatitis virus (immunology), Nitriles (pharmacology), Protein-Serine-Threonine Kinases (antagonists & inhibitors), Protein-Serine-Threonine Kinases (immunology), Protein-Serine-Threonine Kinases (metabolism), Pyridines (pharmacology), Spike Glycoprotein, Coronavirus, Toll-Like Receptor 2 (genetics), Toll-Like Receptor 2 (metabolism), Tumor Necrosis Factor-alpha (agonists), Tumor Necrosis Factor-alpha (metabolism), Viral Envelope Proteins (immunology), Virus Replication (immunology), p38 Mitogen-Activated Protein Kinases (antagonists & inhibitors), p38 Mitogen-Activated Protein Kinases (immunology), p38 Mitogen-Activated Protein Kinases (metabolism).
- MESH :
- chemical , agonists : Interleukin-6, Tumor Necrosis Factor-alpha.
- chemical , antagonists & inhibitors : Protein-Serine-Threonine Kinases, p38 Mitogen-Activated Protein Kinases.
- chemical , biosynthesis : Interleukin-6.
- chemical , genetics : Carcinoembryonic Antigen, Toll-Like Receptor 2.
- chemical , immunology : Heparitin Sulfate, Membrane Glycoproteins, Protein-Serine-Threonine Kinases, Viral Envelope Proteins, p38 Mitogen-Activated Protein Kinases.
- chemical , metabolism : Carcinoembryonic Antigen, Heparitin Sulfate, Protein-Serine-Threonine Kinases, Toll-Like Receptor 2, Tumor Necrosis Factor-alpha, p38 Mitogen-Activated Protein Kinases.
- chemical , pharmacology : Butadienes, Enzyme Inhibitors, Imidazoles, Nitriles, Pyridines.
- complications : Coronavirus Infections.
- drug effects : Fibroblasts, Macrophages, Peritoneal.
- immunology : Hepatitis, Animal, Liver, Macrophages, Peritoneal, Murine hepatitis virus, Virus Replication.
- metabolism : Fibroblasts.
- pathology : Liver.
- virology : Fibroblasts, Hepatitis, Animal, Liver, Macrophages, Peritoneal.
- Animals, Cell Line, Mice, Mice, Knockout, Spike Glycoprotein, Coronavirus.
Abstract
A rapid antiviral immune response may be related to viral interaction with the host cell leading to activation of macrophages via pattern recognition receptors (PPRs) or specific viral receptors. Carcinoembryonic cell adhesion antigen 1a (CEACAM1a) is the specific receptor for the mouse hepatitis virus (MHV), a coronavirus known to induce acute viral hepatitis in mice. The objective of this study was to understand the mechanisms responsible for the secretion of high-pathogenic MHV3-induced inflammatory cytokines. We report that the induction of the pro-inflammatory cytokines interleukin (IL)-6 and tumour necrosis factor (TNF)-alpha in peritoneal macrophages does not depend on CEACAM1a, as demonstrated in cells isolated from Ceacam1a(-/-) mice. The induction of IL-6 and TNF-alpha production was related rather to the fixation of the spike (S) protein of MHV3 on Toll-like receptor 2 (TLR2) in regions enriched in heparan sulphate and did not rely on viral replication, as demonstrated with denatured S protein and UV-inactivated virus. High levels of IL-6 and TNF-alpha were produced in livers from infected C57BL/6 mice but not in livers from Tlr2(-/-) mice. The histopathological observations were correlated with the levels of those inflammatory cytokines. Depending on mouse strain, the viral fixation to heparan sulfate/TLR2 stimulated differently the p38 mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-kappaB in the induction of IL-6 and TNF-alpha. These results suggest that TLR2 and heparan sulphate receptors can act as new viral PPRs involved in inflammatory responses.
DOI: 10.1111/j.1365-2567.2008.02946.x
PubMed: 19740307
Links to Exploration step
pubmed:19740307Le document en format XML
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<author><name sortKey="Jacques, Alexandre" sort="Jacques, Alexandre" uniqKey="Jacques A" first="Alexandre" last="Jacques">Alexandre Jacques</name>
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<author><name sortKey="Turbide, Claire" sort="Turbide, Claire" uniqKey="Turbide C" first="Claire" last="Turbide">Claire Turbide</name>
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<author><name sortKey="Beauchemin, Nicole" sort="Beauchemin, Nicole" uniqKey="Beauchemin N" first="Nicole" last="Beauchemin">Nicole Beauchemin</name>
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<term>Butadienes (pharmacology)</term>
<term>Carcinoembryonic Antigen (genetics)</term>
<term>Carcinoembryonic Antigen (metabolism)</term>
<term>Cell Line</term>
<term>Coronavirus Infections (complications)</term>
<term>Enzyme Inhibitors (pharmacology)</term>
<term>Fibroblasts (drug effects)</term>
<term>Fibroblasts (metabolism)</term>
<term>Fibroblasts (virology)</term>
<term>Heparitin Sulfate (immunology)</term>
<term>Heparitin Sulfate (metabolism)</term>
<term>Hepatitis, Animal (immunology)</term>
<term>Hepatitis, Animal (virology)</term>
<term>Imidazoles (pharmacology)</term>
<term>Interleukin-6 (agonists)</term>
<term>Interleukin-6 (biosynthesis)</term>
<term>Liver (immunology)</term>
<term>Liver (pathology)</term>
<term>Liver (virology)</term>
<term>Macrophages, Peritoneal (drug effects)</term>
<term>Macrophages, Peritoneal (immunology)</term>
<term>Macrophages, Peritoneal (virology)</term>
<term>Membrane Glycoproteins (immunology)</term>
<term>Mice</term>
<term>Mice, Knockout</term>
<term>Murine hepatitis virus (immunology)</term>
<term>Nitriles (pharmacology)</term>
<term>Protein-Serine-Threonine Kinases (antagonists & inhibitors)</term>
<term>Protein-Serine-Threonine Kinases (immunology)</term>
<term>Protein-Serine-Threonine Kinases (metabolism)</term>
<term>Pyridines (pharmacology)</term>
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<term>Toll-Like Receptor 2 (genetics)</term>
<term>Toll-Like Receptor 2 (metabolism)</term>
<term>Tumor Necrosis Factor-alpha (agonists)</term>
<term>Tumor Necrosis Factor-alpha (metabolism)</term>
<term>Viral Envelope Proteins (immunology)</term>
<term>Virus Replication (immunology)</term>
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<term>p38 Mitogen-Activated Protein Kinases (immunology)</term>
<term>p38 Mitogen-Activated Protein Kinases (metabolism)</term>
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<term>Tumor Necrosis Factor-alpha</term>
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<term>p38 Mitogen-Activated Protein Kinases</term>
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<term>Toll-Like Receptor 2</term>
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<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Heparitin Sulfate</term>
<term>Membrane Glycoproteins</term>
<term>Protein-Serine-Threonine Kinases</term>
<term>Viral Envelope Proteins</term>
<term>p38 Mitogen-Activated Protein Kinases</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Carcinoembryonic Antigen</term>
<term>Heparitin Sulfate</term>
<term>Protein-Serine-Threonine Kinases</term>
<term>Toll-Like Receptor 2</term>
<term>Tumor Necrosis Factor-alpha</term>
<term>p38 Mitogen-Activated Protein Kinases</term>
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<term>Enzyme Inhibitors</term>
<term>Imidazoles</term>
<term>Nitriles</term>
<term>Pyridines</term>
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<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Coronavirus Infections</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Fibroblasts</term>
<term>Macrophages, Peritoneal</term>
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<term>Liver</term>
<term>Macrophages, Peritoneal</term>
<term>Murine hepatitis virus</term>
<term>Virus Replication</term>
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<term>Hepatitis, Animal</term>
<term>Liver</term>
<term>Macrophages, Peritoneal</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Line</term>
<term>Mice</term>
<term>Mice, Knockout</term>
<term>Spike Glycoprotein, Coronavirus</term>
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<front><div type="abstract" xml:lang="en">A rapid antiviral immune response may be related to viral interaction with the host cell leading to activation of macrophages via pattern recognition receptors (PPRs) or specific viral receptors. Carcinoembryonic cell adhesion antigen 1a (CEACAM1a) is the specific receptor for the mouse hepatitis virus (MHV), a coronavirus known to induce acute viral hepatitis in mice. The objective of this study was to understand the mechanisms responsible for the secretion of high-pathogenic MHV3-induced inflammatory cytokines. We report that the induction of the pro-inflammatory cytokines interleukin (IL)-6 and tumour necrosis factor (TNF)-alpha in peritoneal macrophages does not depend on CEACAM1a, as demonstrated in cells isolated from Ceacam1a(-/-) mice. The induction of IL-6 and TNF-alpha production was related rather to the fixation of the spike (S) protein of MHV3 on Toll-like receptor 2 (TLR2) in regions enriched in heparan sulphate and did not rely on viral replication, as demonstrated with denatured S protein and UV-inactivated virus. High levels of IL-6 and TNF-alpha were produced in livers from infected C57BL/6 mice but not in livers from Tlr2(-/-) mice. The histopathological observations were correlated with the levels of those inflammatory cytokines. Depending on mouse strain, the viral fixation to heparan sulfate/TLR2 stimulated differently the p38 mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-kappaB in the induction of IL-6 and TNF-alpha. These results suggest that TLR2 and heparan sulphate receptors can act as new viral PPRs involved in inflammatory responses.</div>
</front>
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<ArticleTitle>Macrophage interleukin-6 and tumour necrosis factor-alpha are induced by coronavirus fixation to Toll-like receptor 2/heparan sulphate receptors but not carcinoembryonic cell adhesion antigen 1a.</ArticleTitle>
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<Abstract><AbstractText>A rapid antiviral immune response may be related to viral interaction with the host cell leading to activation of macrophages via pattern recognition receptors (PPRs) or specific viral receptors. Carcinoembryonic cell adhesion antigen 1a (CEACAM1a) is the specific receptor for the mouse hepatitis virus (MHV), a coronavirus known to induce acute viral hepatitis in mice. The objective of this study was to understand the mechanisms responsible for the secretion of high-pathogenic MHV3-induced inflammatory cytokines. We report that the induction of the pro-inflammatory cytokines interleukin (IL)-6 and tumour necrosis factor (TNF)-alpha in peritoneal macrophages does not depend on CEACAM1a, as demonstrated in cells isolated from Ceacam1a(-/-) mice. The induction of IL-6 and TNF-alpha production was related rather to the fixation of the spike (S) protein of MHV3 on Toll-like receptor 2 (TLR2) in regions enriched in heparan sulphate and did not rely on viral replication, as demonstrated with denatured S protein and UV-inactivated virus. High levels of IL-6 and TNF-alpha were produced in livers from infected C57BL/6 mice but not in livers from Tlr2(-/-) mice. The histopathological observations were correlated with the levels of those inflammatory cytokines. Depending on mouse strain, the viral fixation to heparan sulfate/TLR2 stimulated differently the p38 mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-kappaB in the induction of IL-6 and TNF-alpha. These results suggest that TLR2 and heparan sulphate receptors can act as new viral PPRs involved in inflammatory responses.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jacques</LastName>
<ForeName>Alexandre</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Département des Sciences Biologiques, Université du Québec à Montréal, Montréal, QC, Canada.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Bleau</LastName>
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<ForeName>Claire</ForeName>
<Initials>C</Initials>
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<Author ValidYN="Y"><LastName>Beauchemin</LastName>
<ForeName>Nicole</ForeName>
<Initials>N</Initials>
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<Author ValidYN="Y"><LastName>Lamontagne</LastName>
<ForeName>Lucie</ForeName>
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<Language>eng</Language>
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<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
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<ArticleDate DateType="Electronic"><Year>2009</Year>
<Month>08</Month>
<Day>04</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>Immunology</MedlineTA>
<NlmUniqueID>0374672</NlmUniqueID>
<ISSNLinking>0019-2805</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D002070">Butadienes</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D002272">Carcinoembryonic Antigen</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C486183">Ceacam1 protein, mouse</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D004791">Enzyme Inhibitors</NameOfSubstance>
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<NameOfSubstance UI="D007093">Imidazoles</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
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<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C578553">MHV surface projection glycoprotein</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D064370">Spike Glycoprotein, Coronavirus</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D051195">Toll-Like Receptor 2</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D014409">Tumor Necrosis Factor-alpha</NameOfSubstance>
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<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C113580">U 0126</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D014759">Viral Envelope Proteins</NameOfSubstance>
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<MeshHeading><DescriptorName UI="D002272" MajorTopicYN="N">Carcinoembryonic Antigen</DescriptorName>
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<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
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<MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018352" MajorTopicYN="N">Coronavirus Infections</DescriptorName>
<QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName>
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<MeshHeading><DescriptorName UI="D004791" MajorTopicYN="N">Enzyme Inhibitors</DescriptorName>
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<MeshHeading><DescriptorName UI="D005347" MajorTopicYN="N">Fibroblasts</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D006497" MajorTopicYN="N">Heparitin Sulfate</DescriptorName>
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<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
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<MeshHeading><DescriptorName UI="D015850" MajorTopicYN="N">Interleukin-6</DescriptorName>
<QualifierName UI="Q000819" MajorTopicYN="N">agonists</QualifierName>
<QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008099" MajorTopicYN="N">Liver</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
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<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
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<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName>
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<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
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<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
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<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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