MersV1, PubMed, Curation, bibRecord, 001616

Toll-Like Receptor 3 Signaling via TRIF Contributes to a Protective Innate Immune Response to Severe Acute Respiratory Syndrome Coronavirus Infection.

Identifieur interne : 001616 ( PubMed/Curation ); précédent : 001615; suivant : 001617

Toll-Like Receptor 3 Signaling via TRIF Contributes to a Protective Innate Immune Response to Severe Acute Respiratory Syndrome Coronavirus Infection.

Auteurs : Allison L. Totura [États-Unis] ; Alan Whitmore [États-Unis] ; Sudhakar Agnihothram [États-Unis] ; Alexandra Sch Fer [États-Unis] ; Michael G. Katze [États-Unis] ; Mark T. Heise ; Ralph S. Baric [États-Unis]

Source :

mBio [ 2150-7511 ] ; 2015.

RBID : pubmed:26015500

Descripteurs français

KwdFr :
- Analyse de survie, Animaux, Charge virale, Immunité innée, Poids du corps, Poumon (anatomopathologie), Poumon (physiopathologie), Protéines adaptatrices du transport vésiculaire (déficit), Protéines adaptatrices du transport vésiculaire (métabolisme), Récepteur de type Toll-3 (déficit), Récepteur de type Toll-3 (métabolisme), Récepteur de type Toll-4 (déficit), Récepteur de type Toll-4 (métabolisme), Récepteurs aux interleukines (déficit), Récepteurs aux interleukines (métabolisme), Souris knockout, Susceptibilité à une maladie, Tests de la fonction respiratoire, Transduction du signal, Virus du SRAS (immunologie).
MESH :
- anatomopathologie : Poumon.
- déficit : Protéines adaptatrices du transport vésiculaire, Récepteur de type Toll-3, Récepteur de type Toll-4, Récepteurs aux interleukines.
- immunologie : Virus du SRAS.
- métabolisme : Protéines adaptatrices du transport vésiculaire, Récepteur de type Toll-3, Récepteur de type Toll-4, Récepteurs aux interleukines.
- physiopathologie : Poumon.
- Analyse de survie, Animaux, Charge virale, Immunité innée, Poids du corps, Souris knockout, Susceptibilité à une maladie, Tests de la fonction respiratoire, Transduction du signal.

English descriptors

KwdEn :
- Adaptor Proteins, Vesicular Transport (deficiency), Adaptor Proteins, Vesicular Transport (metabolism), Animals, Body Weight, Disease Susceptibility, Immunity, Innate, Lung (pathology), Lung (physiopathology), Mice, Knockout, Receptors, Interleukin (deficiency), Receptors, Interleukin (metabolism), Respiratory Function Tests, SARS Virus (immunology), Signal Transduction, Survival Analysis, Toll-Like Receptor 3 (deficiency), Toll-Like Receptor 3 (metabolism), Toll-Like Receptor 4 (deficiency), Toll-Like Receptor 4 (metabolism), Viral Load.
MESH :
- chemical , deficiency : Adaptor Proteins, Vesicular Transport, Receptors, Interleukin, Toll-Like Receptor 3, Toll-Like Receptor 4.
- chemical , metabolism : Adaptor Proteins, Vesicular Transport, Receptors, Interleukin, Toll-Like Receptor 3, Toll-Like Receptor 4.
- immunology : SARS Virus.
- pathology : Lung.
- physiopathology : Lung.
- Animals, Body Weight, Disease Susceptibility, Immunity, Innate, Mice, Knockout, Respiratory Function Tests, Signal Transduction, Survival Analysis, Viral Load.

Abstract

Toll-like receptors (TLRs) are sensors that recognize molecular patterns from viruses, bacteria, and fungi to initiate innate immune responses to invading pathogens. The emergence of highly pathogenic coronaviruses severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) is a concern for global public health, as there is a lack of efficacious vaccine platforms and antiviral therapeutic strategies. Previously, it was shown that MyD88, an adaptor protein necessary for signaling by multiple TLRs, is a required component of the innate immune response to mouse-adapted SARS-CoV infection in vivo. Here, we demonstrate that TLR3(-/-), TLR4(-/-), and TRAM(-/-) mice are more susceptible to SARS-CoV than wild-type mice but experience only transient weight loss with no mortality in response to infection. In contrast, mice deficient in the TLR3/TLR4 adaptor TRIF are highly susceptible to SARS-CoV infection, showing increased weight loss, mortality, reduced lung function, increased lung pathology, and higher viral titers. Distinct alterations in inflammation were present in TRIF(-/-) mice infected with SARS-CoV, including excess infiltration of neutrophils and inflammatory cell types that correlate with increased pathology of other known causes of acute respiratory distress syndrome (ARDS), including influenza virus infections. Aberrant proinflammatory cytokine, chemokine, and interferon-stimulated gene (ISG) signaling programs were also noted following infection of TRIF(-/-) mice that were similar to those seen in human patients with poor disease outcome following SARS-CoV or MERS-CoV infection. These findings highlight the importance of TLR adaptor signaling in generating a balanced protective innate immune response to highly pathogenic coronavirus infections.

DOI: 10.1128/mBio.00638-15
PubMed: 26015500

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Le document en format XML

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<term>Animals</term>
<term>Body Weight</term>
<term>Disease Susceptibility</term>
<term>Immunity, Innate</term>
<term>Lung (pathology)</term>
<term>Lung (physiopathology)</term>
<term>Mice, Knockout</term>
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<term>Toll-Like Receptor 3 (metabolism)</term>
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<term>Animaux</term>
<term>Charge virale</term>
<term>Immunité innée</term>
<term>Poids du corps</term>
<term>Poumon (anatomopathologie)</term>
<term>Poumon (physiopathologie)</term>
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<term>Receptors, Interleukin</term>
<term>Toll-Like Receptor 3</term>
<term>Toll-Like Receptor 4</term>
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<term>Receptors, Interleukin</term>
<term>Toll-Like Receptor 3</term>
<term>Toll-Like Receptor 4</term>
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<term>Récepteur de type Toll-4</term>
<term>Récepteurs aux interleukines</term>
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<term>Récepteur de type Toll-4</term>
<term>Récepteurs aux interleukines</term>
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<term>Viral Load</term>
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<term>Immunité innée</term>
<term>Poids du corps</term>
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<front><div type="abstract" xml:lang="en">Toll-like receptors (TLRs) are sensors that recognize molecular patterns from viruses, bacteria, and fungi to initiate innate immune responses to invading pathogens. The emergence of highly pathogenic coronaviruses severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) is a concern for global public health, as there is a lack of efficacious vaccine platforms and antiviral therapeutic strategies. Previously, it was shown that MyD88, an adaptor protein necessary for signaling by multiple TLRs, is a required component of the innate immune response to mouse-adapted SARS-CoV infection in vivo. Here, we demonstrate that TLR3(-/-), TLR4(-/-), and TRAM(-/-) mice are more susceptible to SARS-CoV than wild-type mice but experience only transient weight loss with no mortality in response to infection. In contrast, mice deficient in the TLR3/TLR4 adaptor TRIF are highly susceptible to SARS-CoV infection, showing increased weight loss, mortality, reduced lung function, increased lung pathology, and higher viral titers. Distinct alterations in inflammation were present in TRIF(-/-) mice infected with SARS-CoV, including excess infiltration of neutrophils and inflammatory cell types that correlate with increased pathology of other known causes of acute respiratory distress syndrome (ARDS), including influenza virus infections. Aberrant proinflammatory cytokine, chemokine, and interferon-stimulated gene (ISG) signaling programs were also noted following infection of TRIF(-/-) mice that were similar to those seen in human patients with poor disease outcome following SARS-CoV or MERS-CoV infection. These findings highlight the importance of TLR adaptor signaling in generating a balanced protective innate immune response to highly pathogenic coronavirus infections.</div>
</front>
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<Month>01</Month>
<Day>11</Day>
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<Month>04</Month>
<Day>04</Day>
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<Issue>3</Issue>
<PubDate><Year>2015</Year>
<Month>May</Month>
<Day>26</Day>
</PubDate>
</JournalIssue>
<Title>mBio</Title>
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<ArticleTitle>Toll-Like Receptor 3 Signaling via TRIF Contributes to a Protective Innate Immune Response to Severe Acute Respiratory Syndrome Coronavirus Infection.</ArticleTitle>
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<Abstract><AbstractText Label="UNLABELLED">Toll-like receptors (TLRs) are sensors that recognize molecular patterns from viruses, bacteria, and fungi to initiate innate immune responses to invading pathogens. The emergence of highly pathogenic coronaviruses severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) is a concern for global public health, as there is a lack of efficacious vaccine platforms and antiviral therapeutic strategies. Previously, it was shown that MyD88, an adaptor protein necessary for signaling by multiple TLRs, is a required component of the innate immune response to mouse-adapted SARS-CoV infection in vivo. Here, we demonstrate that TLR3(-/-), TLR4(-/-), and TRAM(-/-) mice are more susceptible to SARS-CoV than wild-type mice but experience only transient weight loss with no mortality in response to infection. In contrast, mice deficient in the TLR3/TLR4 adaptor TRIF are highly susceptible to SARS-CoV infection, showing increased weight loss, mortality, reduced lung function, increased lung pathology, and higher viral titers. Distinct alterations in inflammation were present in TRIF(-/-) mice infected with SARS-CoV, including excess infiltration of neutrophils and inflammatory cell types that correlate with increased pathology of other known causes of acute respiratory distress syndrome (ARDS), including influenza virus infections. Aberrant proinflammatory cytokine, chemokine, and interferon-stimulated gene (ISG) signaling programs were also noted following infection of TRIF(-/-) mice that were similar to those seen in human patients with poor disease outcome following SARS-CoV or MERS-CoV infection. These findings highlight the importance of TLR adaptor signaling in generating a balanced protective innate immune response to highly pathogenic coronavirus infections.</AbstractText>
<AbstractText Label="IMPORTANCE" NlmCategory="OBJECTIVE">Toll-like receptors are a family of sensor proteins that enable the immune system to differentiate between "self" and "non-self." Agonists and antagonists of TLRs have been proposed to have utility as vaccine adjuvants or antiviral compounds. In the last 15 years, the emergence of highly pathogenic coronaviruses SARS-CoV and MERS-CoV has caused significant disease accompanied by high mortality rates in human populations, but no approved therapeutic treatments or vaccines currently exist. Here, we demonstrate that TLR signaling through the TRIF adaptor protein protects mice from lethal SARS-CoV disease. Our findings indicate that a balanced immune response operating through both TRIF-driven and MyD88-driven pathways likely provides the most effective host cell intrinsic antiviral defense responses to severe SARS-CoV disease, while removal of either branch of TLR signaling causes lethal SARS-CoV disease in our mouse model. These data should inform the design and use of TLR agonists and antagonists in coronavirus-specific vaccine and antiviral strategies.</AbstractText>
<CopyrightInformation>Copyright © 2015 Totura et al.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Totura</LastName>
<ForeName>Allison L</ForeName>
<Initials>AL</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of North Carolina-Chapel Hill, Chapel Hill, North Carolina, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Whitmore</LastName>
<ForeName>Alan</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Genetics, University of North Carolina-Chapel Hill, Chapel Hill, North Carolina, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Agnihothram</LastName>
<ForeName>Sudhakar</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Epidemiology, University of North Carolina-Chapel Hill, Chapel Hill, North Carolina, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Schäfer</LastName>
<ForeName>Alexandra</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Epidemiology, University of North Carolina-Chapel Hill, Chapel Hill, North Carolina, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Katze</LastName>
<ForeName>Michael G</ForeName>
<Initials>MG</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology, University of Washington, Seattle, Washington, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Heise</LastName>
<ForeName>Mark T</ForeName>
<Initials>MT</Initials>
</Author>
<Author ValidYN="Y"><LastName>Baric</LastName>
<ForeName>Ralph S</ForeName>
<Initials>RS</Initials>
<AffiliationInfo><Affiliation>rbaric@email.unc.edu.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
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<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
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<Grant><GrantID>P51 OD010425</GrantID>
<Acronym>OD</Acronym>
<Agency>NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>U19 AI100625</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>U19 AI106772</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
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<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
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<ArticleDate DateType="Electronic"><Year>2015</Year>
<Month>05</Month>
<Day>26</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>mBio</MedlineTA>
<NlmUniqueID>101519231</NlmUniqueID>
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<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D033942">Adaptor Proteins, Vesicular Transport</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D018123">Receptors, Interleukin</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C476286">TICAM-1 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C476416">TIRP protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
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</Chemical>
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<NameOfSubstance UI="C493487">Tlr4 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D051196">Toll-Like Receptor 3</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D051197">Toll-Like Receptor 4</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>MBio. 2015;6(4):e01120</RefSource>
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Toll-Like Receptor 3 Signaling via TRIF Contributes to a Protective Innate Immune Response to Severe Acute Respiratory Syndrome Coronavirus Infection.

Toll-Like Receptor 3 Signaling via TRIF Contributes to a Protective Innate Immune Response to Severe Acute Respiratory Syndrome Coronavirus Infection.

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