Mouse-Passaged Severe Acute Respiratory Syndrome-Associated Coronavirus Leads to Lethal Pulmonary Edema and Diffuse Alveolar Damage in Adult but Not Young Mice
Identifieur interne : 003486 ( Main/Exploration ); précédent : 003485; suivant : 003487Mouse-Passaged Severe Acute Respiratory Syndrome-Associated Coronavirus Leads to Lethal Pulmonary Edema and Diffuse Alveolar Damage in Adult but Not Young Mice
Auteurs : Noriyo Nagata [Japon] ; Naoko Iwata [Japon] ; Hideki Hasegawa [Japon] ; Shuetsu Fukushi [Japon] ; Ayako Harashima [Japon] ; Yuko Sato [Japon] ; Masayuki Saijo [Japon] ; Fumihiro Taguchi [Japon] ; Shigeru Morikawa [Japon] ; Tetsutaro Sata [Japon]Source :
- The American journal of pathology [ 0002-9440 ] ; 2008.
Descripteurs français
- KwdFr :
- Alvéoles pulmonaires (anatomopathologie), Alvéoles pulmonaires (virologie), Animaux, Cytokines (métabolisme), Femelle, Humains, Modèles animaux de maladie humaine, Oedème pulmonaire (anatomopathologie), Oedème pulmonaire (immunologie), Oedème pulmonaire (virologie), Réplication virale, Souris, Souris de lignée BALB C, Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (virologie), Vieillissement (anatomopathologie), Vieillissement (immunologie), Virus du SRAS (immunologie), Virus du SRAS (physiologie).
- MESH :
- anatomopathologie : Alvéoles pulmonaires, Oedème pulmonaire, Syndrome respiratoire aigu sévère, Vieillissement.
- immunologie : Oedème pulmonaire, Syndrome respiratoire aigu sévère, Vieillissement, Virus du SRAS.
- métabolisme : Cytokines.
- physiologie : Virus du SRAS.
- virologie : Alvéoles pulmonaires, Oedème pulmonaire, Syndrome respiratoire aigu sévère.
- Pascal (Inist)
- Wicri :
- topic : Mortalité.
English descriptors
- KwdEn :
- Adult animal, Aging (immunology), Aging (pathology), Anatomic pathology, Animals, Coronavirus, Cytokines (metabolism), Diffuse, Disease Models, Animal, Female, Humans, Lesion, Lung edema, Mice, Mice, Inbred BALB C, Mortality, Mouse, Pulmonary Alveoli (pathology), Pulmonary Alveoli (virology), Pulmonary Edema (immunology), Pulmonary Edema (pathology), Pulmonary Edema (virology), SARS Virus (immunology), SARS Virus (physiology), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (pathology), Severe Acute Respiratory Syndrome (virology), Severe acute respiratory syndrome, Virus Replication.
- MESH :
- chemical , metabolism : Cytokines.
- immunology : Aging, Pulmonary Edema, SARS Virus, Severe Acute Respiratory Syndrome.
- pathology : Aging, Pulmonary Alveoli, Pulmonary Edema, Severe Acute Respiratory Syndrome.
- physiology : SARS Virus.
- virology : Pulmonary Alveoli, Pulmonary Edema, Severe Acute Respiratory Syndrome.
- Animals, Disease Models, Animal, Female, Humans, Mice, Mice, Inbred BALB C, Virus Replication.
Abstract
Advanced age is a risk factor of severe acute respiratory syndrome (SARS) in humans. To understand its pathogenesis, we developed an animal model using BALB/c mice and the mouse-passaged Frankfurt 1 isolate of SARS coronavirus (SARS-CoV). We examined the immune responses to SARS-CoV in both young and adult mice. SARS-CoV induced severe respiratory illness in all adult, but not young, mice on day 2 after inoculation with a mortality rate of 30 to 50%. Moribund adult mice showed severe pulmonary edema and diffuse alveolar damage accompanied by virus replication. Adult murine lungs, which had significantly higher interleukin (IL)-4 and lower IL-10 and IL-13 levels before infection than young murine lungs, rapidly produced high levels of proinflammatory chemokines and cytokines known to induce macrophage and neutrophil infiltration and activation (eg, tumor necrosis factor-a). On day 2 after inoculation, young murine lungs produced not only proinflammatory cytokines but also IL-2, interferon-y, IL-10, and IL-13. Adult mice showed early and acute excessive proinflammatory responses (ie, cytokine storm) in the lungs after SARS-CoV infection, which led to severe pulmonary edema and diffuse alveolar damage. Intravenous injection with anti-tumor necrosis factor-a antibody 3 hours after infection had no effect on SARS-CoV infection. However, intraperitoneal interferon-y injection protected adult mice from the lethal respiratory illness. The experimental model described here may be useful for elucidating the pathophysiology of SARS and for evaluating therapies to treat SARS-CoV infection.
Url:
Affiliations:
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Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult animal</term>
<term>Aging (immunology)</term>
<term>Aging (pathology)</term>
<term>Anatomic pathology</term>
<term>Animals</term>
<term>Coronavirus</term>
<term>Cytokines (metabolism)</term>
<term>Diffuse</term>
<term>Disease Models, Animal</term>
<term>Female</term>
<term>Humans</term>
<term>Lesion</term>
<term>Lung edema</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Mortality</term>
<term>Mouse</term>
<term>Pulmonary Alveoli (pathology)</term>
<term>Pulmonary Alveoli (virology)</term>
<term>Pulmonary Edema (immunology)</term>
<term>Pulmonary Edema (pathology)</term>
<term>Pulmonary Edema (virology)</term>
<term>SARS Virus (immunology)</term>
<term>SARS Virus (physiology)</term>
<term>Severe Acute Respiratory Syndrome (immunology)</term>
<term>Severe Acute Respiratory Syndrome (pathology)</term>
<term>Severe Acute Respiratory Syndrome (virology)</term>
<term>Severe acute respiratory syndrome</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Alvéoles pulmonaires (anatomopathologie)</term>
<term>Alvéoles pulmonaires (virologie)</term>
<term>Animaux</term>
<term>Cytokines (métabolisme)</term>
<term>Femelle</term>
<term>Humains</term>
<term>Modèles animaux de maladie humaine</term>
<term>Oedème pulmonaire (anatomopathologie)</term>
<term>Oedème pulmonaire (immunologie)</term>
<term>Oedème pulmonaire (virologie)</term>
<term>Réplication virale</term>
<term>Souris</term>
<term>Souris de lignée BALB C</term>
<term>Syndrome respiratoire aigu sévère (anatomopathologie)</term>
<term>Syndrome respiratoire aigu sévère (immunologie)</term>
<term>Syndrome respiratoire aigu sévère (virologie)</term>
<term>Vieillissement (anatomopathologie)</term>
<term>Vieillissement (immunologie)</term>
<term>Virus du SRAS (immunologie)</term>
<term>Virus du SRAS (physiologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Alvéoles pulmonaires</term>
<term>Oedème pulmonaire</term>
<term>Syndrome respiratoire aigu sévère</term>
<term>Vieillissement</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Oedème pulmonaire</term>
<term>Syndrome respiratoire aigu sévère</term>
<term>Vieillissement</term>
<term>Virus du SRAS</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Aging</term>
<term>Pulmonary Edema</term>
<term>SARS Virus</term>
<term>Severe Acute Respiratory Syndrome</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cytokines</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Aging</term>
<term>Pulmonary Alveoli</term>
<term>Pulmonary Edema</term>
<term>Severe Acute Respiratory Syndrome</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Virus du SRAS</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>SARS Virus</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Alvéoles pulmonaires</term>
<term>Oedème pulmonaire</term>
<term>Syndrome respiratoire aigu sévère</term>
</keywords>
<keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Pulmonary Alveoli</term>
<term>Pulmonary Edema</term>
<term>Severe Acute Respiratory Syndrome</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Disease Models, Animal</term>
<term>Female</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Animaux</term>
<term>Femelle</term>
<term>Humains</term>
<term>Modèles animaux de maladie humaine</term>
<term>Oedème du poumon</term>
<term>Réplication virale</term>
<term>Souris</term>
<term>Animal adulte</term>
<term>Souris de lignée BALB C</term>
<term>Syndrome respiratoire aigu sévère</term>
<term>Coronavirus</term>
<term>Mortalité</term>
<term>Diffus</term>
<term>Lésion</term>
<term>Anatomopathologie</term>
</keywords>
<keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Mortalité</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Advanced age is a risk factor of severe acute respiratory syndrome (SARS) in humans. To understand its pathogenesis, we developed an animal model using BALB/c mice and the mouse-passaged Frankfurt 1 isolate of SARS coronavirus (SARS-CoV). We examined the immune responses to SARS-CoV in both young and adult mice. SARS-CoV induced severe respiratory illness in all adult, but not young, mice on day 2 after inoculation with a mortality rate of 30 to 50%. Moribund adult mice showed severe pulmonary edema and diffuse alveolar damage accompanied by virus replication. Adult murine lungs, which had significantly higher interleukin (IL)-4 and lower IL-10 and IL-13 levels before infection than young murine lungs, rapidly produced high levels of proinflammatory chemokines and cytokines known to induce macrophage and neutrophil infiltration and activation (eg, tumor necrosis factor-a). On day 2 after inoculation, young murine lungs produced not only proinflammatory cytokines but also IL-2, interferon-y, IL-10, and IL-13. Adult mice showed early and acute excessive proinflammatory responses (ie, cytokine storm) in the lungs after SARS-CoV infection, which led to severe pulmonary edema and diffuse alveolar damage. Intravenous injection with anti-tumor necrosis factor-a antibody 3 hours after infection had no effect on SARS-CoV infection. However, intraperitoneal interferon-y injection protected adult mice from the lethal respiratory illness. The experimental model described here may be useful for elucidating the pathophysiology of SARS and for evaluating therapies to treat SARS-CoV infection.</div>
</front>
</TEI>
<affiliations><list><country><li>Japon</li>
</country>
<region><li>Région de Kantō</li>
</region>
<settlement><li>Tokyo</li>
</settlement>
</list>
<tree><country name="Japon"><region name="Région de Kantō"><name sortKey="Nagata, Noriyo" sort="Nagata, Noriyo" uniqKey="Nagata N" first="Noriyo" last="Nagata">Noriyo Nagata</name>
</region>
<name sortKey="Fukushi, Shuetsu" sort="Fukushi, Shuetsu" uniqKey="Fukushi S" first="Shuetsu" last="Fukushi">Shuetsu Fukushi</name>
<name sortKey="Harashima, Ayako" sort="Harashima, Ayako" uniqKey="Harashima A" first="Ayako" last="Harashima">Ayako Harashima</name>
<name sortKey="Hasegawa, Hideki" sort="Hasegawa, Hideki" uniqKey="Hasegawa H" first="Hideki" last="Hasegawa">Hideki Hasegawa</name>
<name sortKey="Iwata, Naoko" sort="Iwata, Naoko" uniqKey="Iwata N" first="Naoko" last="Iwata">Naoko Iwata</name>
<name sortKey="Morikawa, Shigeru" sort="Morikawa, Shigeru" uniqKey="Morikawa S" first="Shigeru" last="Morikawa">Shigeru Morikawa</name>
<name sortKey="Saijo, Masayuki" sort="Saijo, Masayuki" uniqKey="Saijo M" first="Masayuki" last="Saijo">Masayuki Saijo</name>
<name sortKey="Sata, Tetsutaro" sort="Sata, Tetsutaro" uniqKey="Sata T" first="Tetsutaro" last="Sata">Tetsutaro Sata</name>
<name sortKey="Sato, Yuko" sort="Sato, Yuko" uniqKey="Sato Y" first="Yuko" last="Sato">Yuko Sato</name>
<name sortKey="Taguchi, Fumihiro" sort="Taguchi, Fumihiro" uniqKey="Taguchi F" first="Fumihiro" last="Taguchi">Fumihiro Taguchi</name>
</country>
</tree>
</affiliations>
</record>
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