Toll-Like Receptor 3 Signaling via TRIF Contributes to a Protective Innate Immune Response to Severe Acute Respiratory Syndrome Coronavirus Infection
Identifieur interne : 001213 ( Main/Merge ); précédent : 001212; suivant : 001214Toll-Like Receptor 3 Signaling via TRIF Contributes to a Protective Innate Immune Response to Severe Acute Respiratory Syndrome Coronavirus Infection
Auteurs : Allison L. Totura ; Alan Whitmore ; Sudhakar Agnihothram ; Alexandra Sch Fer ; Michael G. Katze ; Mark T. Heise ; Ralph S. BaricSource :
- mBio [ 2150-7511 ] ; 2015.
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
Url:
DOI: 10.1128/mBio.00638-15
PubMed: 26015500
PubMed Central: 4447251
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Links to Exploration step
PMC:4447251Le document en format XML
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<term>Adaptor Proteins, Vesicular Transport (metabolism)</term>
<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>
<term>Receptors, Interleukin (deficiency)</term>
<term>Receptors, Interleukin (metabolism)</term>
<term>Respiratory Function Tests</term>
<term>SARS Virus (immunology)</term>
<term>Signal Transduction</term>
<term>Survival Analysis</term>
<term>Toll-Like Receptor 3 (deficiency)</term>
<term>Toll-Like Receptor 3 (metabolism)</term>
<term>Toll-Like Receptor 4 (deficiency)</term>
<term>Toll-Like Receptor 4 (metabolism)</term>
<term>Viral Load</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Analyse de survie</term>
<term>Animaux</term>
<term>Charge virale</term>
<term>Immunité innée</term>
<term>Poids du corps</term>
<term>Poumon (anatomopathologie)</term>
<term>Poumon (physiopathologie)</term>
<term>Protéines adaptatrices du transport vésiculaire (déficit)</term>
<term>Protéines adaptatrices du transport vésiculaire (métabolisme)</term>
<term>Récepteur de type Toll-3 (déficit)</term>
<term>Récepteur de type Toll-3 (métabolisme)</term>
<term>Récepteur de type Toll-4 (déficit)</term>
<term>Récepteur de type Toll-4 (métabolisme)</term>
<term>Récepteurs aux interleukines (déficit)</term>
<term>Récepteurs aux interleukines (métabolisme)</term>
<term>Souris knockout</term>
<term>Susceptibilité à une maladie</term>
<term>Tests de la fonction respiratoire</term>
<term>Transduction du signal</term>
<term>Virus du SRAS (immunologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Adaptor Proteins, Vesicular Transport</term>
<term>Receptors, Interleukin</term>
<term>Toll-Like Receptor 3</term>
<term>Toll-Like Receptor 4</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adaptor Proteins, Vesicular Transport</term>
<term>Receptors, Interleukin</term>
<term>Toll-Like Receptor 3</term>
<term>Toll-Like Receptor 4</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Protéines adaptatrices du transport vésiculaire</term>
<term>Récepteur de type Toll-3</term>
<term>Récepteur de type Toll-4</term>
<term>Récepteurs aux interleukines</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Virus du SRAS</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>SARS Virus</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Protéines adaptatrices du transport vésiculaire</term>
<term>Récepteur de type Toll-3</term>
<term>Récepteur de type Toll-4</term>
<term>Récepteurs aux interleukines</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Lung</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Body Weight</term>
<term>Disease Susceptibility</term>
<term>Immunity, Innate</term>
<term>Mice, Knockout</term>
<term>Respiratory Function Tests</term>
<term>Signal Transduction</term>
<term>Survival Analysis</term>
<term>Viral Load</term>
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<term>Animaux</term>
<term>Charge virale</term>
<term>Immunité innée</term>
<term>Poids du corps</term>
<term>Souris knockout</term>
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<front><div type="abstract" xml:lang="en"><title>ABSTRACT</title>
<p>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 <italic>in vivo</italic>
. Here, we demonstrate that TLR3<sup>−/−</sup>
, TLR4<sup>−/−</sup>
, and TRAM<sup>−/−</sup>
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<sup>−/−</sup>
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<sup>−/−</sup>
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.</p>
</div>
</front>
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