EMAPII Monoclonal Antibody Ameliorates Influenza A Virus-Induced Lung Injury.
Identifieur interne : 000A07 ( Main/Exploration ); précédent : 000A06; suivant : 000A08EMAPII Monoclonal Antibody Ameliorates Influenza A Virus-Induced Lung Injury.
Auteurs : Hongyan Lu [États-Unis] ; Sarvesh Chelvanambi [États-Unis] ; Christophe Poirier [États-Unis] ; Jacob Saliba [États-Unis] ; Keith L. March [États-Unis] ; Matthias Clauss [États-Unis] ; Natalia V. Bogatcheva [États-Unis]Source :
- Molecular therapy : the journal of the American Society of Gene Therapy [ 1525-0024 ] ; 2018.
Descripteurs français
- KwdFr :
- Animaux, Anticorps monoclonaux (administration et posologie), Anticorps monoclonaux (pharmacologie), Caspase-3, Grippe humaine (métabolisme), Grippe humaine (traitement médicamenteux), Humains, Injections, Lignée cellulaire, Liquide de lavage bronchoalvéolaire (), Liquide de lavage bronchoalvéolaire (virologie), Lésion pulmonaire (métabolisme), Lésion pulmonaire (traitement médicamenteux), Lésion pulmonaire (virologie), Modèles animaux de maladie humaine, Perte de poids (), Protéines associées aux microtubules (métabolisme), Résultat thérapeutique, Souris, Transport de protéines (), Virus de la grippe A ().
- MESH :
- administration et posologie : Anticorps monoclonaux.
- métabolisme : Grippe humaine, Lésion pulmonaire, Protéines associées aux microtubules.
- pharmacologie : Anticorps monoclonaux.
- traitement médicamenteux : Grippe humaine, Lésion pulmonaire.
- virologie : Liquide de lavage bronchoalvéolaire, Lésion pulmonaire.
- Animaux, Caspase-3, Humains, Injections, Lignée cellulaire, Liquide de lavage bronchoalvéolaire, Modèles animaux de maladie humaine, Perte de poids, Résultat thérapeutique, Souris, Transport de protéines, Virus de la grippe A.
English descriptors
- KwdEn :
- Animals, Antibodies, Monoclonal (administration & dosage), Antibodies, Monoclonal (pharmacology), Bronchoalveolar Lavage Fluid (chemistry), Bronchoalveolar Lavage Fluid (virology), Caspase 3, Cell Line, Disease Models, Animal, Humans, Influenza A virus (drug effects), Influenza, Human (drug therapy), Influenza, Human (metabolism), Injections, Lung Injury (drug therapy), Lung Injury (metabolism), Lung Injury (virology), Mice, Microtubule-Associated Proteins (metabolism), Protein Transport (drug effects), Treatment Outcome, Weight Loss (drug effects).
- MESH :
- chemical , administration & dosage : Antibodies, Monoclonal.
- chemical , metabolism : Microtubule-Associated Proteins.
- chemical , pharmacology : Antibodies, Monoclonal.
- chemistry : Bronchoalveolar Lavage Fluid.
- drug effects : Influenza A virus, Protein Transport, Weight Loss.
- drug therapy : Influenza, Human, Lung Injury.
- metabolism : Influenza, Human, Lung Injury.
- virology : Bronchoalveolar Lavage Fluid, Lung Injury.
- Animals, Caspase 3, Cell Line, Disease Models, Animal, Humans, Injections, Mice, Treatment Outcome.
Abstract
Influenza A virus (IAV) remains a major worldwide health threat, especially to high-risk populations, including the young and elderly. There is an unmet clinical need for therapy that will protect the lungs from damage caused by lower respiratory infection. Here, we analyzed the role of EMAPII, a stress- and virus-induced pro-inflammatory and pro-apoptotic factor, in IAV-induced lung injury. First, we demonstrated that IAV induces EMAPII surface translocation, release, and apoptosis in cultured endothelial and epithelial cells. Next, we showed that IAV induces EMAPII surface translocation and release to bronchoalveolar lavage fluid (BALF) in mouse lungs, concomitant with increases in caspase 3 activity. Injection of monoclonal antibody (mAb) against EMAPII attenuated IAV-induced EMAPII levels, weight loss, reduction of blood oxygenation, lung edema, and increase of the pro-inflammatory cytokine TNF alpha. In accordance with the pro-apoptotic properties of EMAPII, levels of caspase 3 activity in BALF were also decreased by mAb treatment. Moreover, we detected EMAPII mAb-induced increase in lung levels of M2-like macrophage markers YM1 and CD206. All together, these data strongly suggest that EMAPII mAb ameliorates IAV-induced lung injury by limiting lung cell apoptosis and shifting the host inflammatory setting toward resolution of inflammation.
DOI: 10.1016/j.ymthe.2018.05.017
PubMed: 29910176
Affiliations:
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Bogatcheva</name><affiliation wicri:level="2"><nlm:affiliation>Division of Cardiology, Indiana University School of Medicine, Indianapolis, IN, USA; VC-CAST Signature Center, Indianapolis, IN, USA; Roudebush Veterans Affairs Medical Center, Indiana University, Indianapolis, IN, USA. Electronic address: nbogatch@iu.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Cardiology, Indiana University School of Medicine, Indianapolis, IN, USA; VC-CAST Signature Center, Indianapolis, IN, USA; Roudebush Veterans Affairs Medical Center, Indiana University, Indianapolis, IN</wicri:regionArea><placeName><region type="state">Indiana</region></placeName></affiliation></author></analytic><series><title level="j">Molecular therapy : the journal of the American Society of Gene Therapy</title><idno type="eISSN">1525-0024</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antibodies, Monoclonal (administration & dosage)</term><term>Antibodies, Monoclonal (pharmacology)</term><term>Bronchoalveolar Lavage Fluid (chemistry)</term><term>Bronchoalveolar Lavage Fluid (virology)</term><term>Caspase 3</term><term>Cell Line</term><term>Disease Models, Animal</term><term>Humans</term><term>Influenza A virus (drug effects)</term><term>Influenza, Human (drug therapy)</term><term>Influenza, Human (metabolism)</term><term>Injections</term><term>Lung Injury (drug therapy)</term><term>Lung Injury (metabolism)</term><term>Lung Injury (virology)</term><term>Mice</term><term>Microtubule-Associated Proteins (metabolism)</term><term>Protein Transport (drug effects)</term><term>Treatment Outcome</term><term>Weight Loss (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Anticorps monoclonaux (administration et posologie)</term><term>Anticorps monoclonaux (pharmacologie)</term><term>Caspase-3</term><term>Grippe humaine (métabolisme)</term><term>Grippe humaine (traitement médicamenteux)</term><term>Humains</term><term>Injections</term><term>Lignée cellulaire</term><term>Liquide de lavage bronchoalvéolaire ()</term><term>Liquide de lavage bronchoalvéolaire (virologie)</term><term>Lésion pulmonaire (métabolisme)</term><term>Lésion pulmonaire (traitement médicamenteux)</term><term>Lésion pulmonaire (virologie)</term><term>Modèles animaux de maladie humaine</term><term>Perte de poids ()</term><term>Protéines associées aux microtubules (métabolisme)</term><term>Résultat thérapeutique</term><term>Souris</term><term>Transport de protéines ()</term><term>Virus de la grippe A ()</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Antibodies, Monoclonal</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Microtubule-Associated Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antibodies, Monoclonal</term></keywords><keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Anticorps 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scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Liquide de lavage bronchoalvéolaire</term><term>Lésion pulmonaire</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Bronchoalveolar Lavage Fluid</term><term>Lung Injury</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Caspase 3</term><term>Cell Line</term><term>Disease Models, Animal</term><term>Humans</term><term>Injections</term><term>Mice</term><term>Treatment Outcome</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Caspase-3</term><term>Humains</term><term>Injections</term><term>Lignée cellulaire</term><term>Liquide de lavage bronchoalvéolaire</term><term>Modèles animaux de maladie humaine</term><term>Perte de poids</term><term>Résultat thérapeutique</term><term>Souris</term><term>Transport de protéines</term><term>Virus de la grippe A</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Influenza A virus (IAV) remains a major worldwide health threat, especially to high-risk populations, including the young and elderly. There is an unmet clinical need for therapy that will protect the lungs from damage caused by lower respiratory infection. Here, we analyzed the role of EMAPII, a stress- and virus-induced pro-inflammatory and pro-apoptotic factor, in IAV-induced lung injury. First, we demonstrated that IAV induces EMAPII surface translocation, release, and apoptosis in cultured endothelial and epithelial cells. Next, we showed that IAV induces EMAPII surface translocation and release to bronchoalveolar lavage fluid (BALF) in mouse lungs, concomitant with increases in caspase 3 activity. Injection of monoclonal antibody (mAb) against EMAPII attenuated IAV-induced EMAPII levels, weight loss, reduction of blood oxygenation, lung edema, and increase of the pro-inflammatory cytokine TNF alpha. In accordance with the pro-apoptotic properties of EMAPII, levels of caspase 3 activity in BALF were also decreased by mAb treatment. Moreover, we detected EMAPII mAb-induced increase in lung levels of M2-like macrophage markers YM1 and CD206. All together, these data strongly suggest that EMAPII mAb ameliorates IAV-induced lung injury by limiting lung cell apoptosis and shifting the host inflammatory setting toward resolution of inflammation.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Indiana</li></region></list><tree><country name="États-Unis"><region name="Indiana"><name sortKey="Lu, Hongyan" sort="Lu, Hongyan" uniqKey="Lu H" first="Hongyan" last="Lu">Hongyan Lu</name></region><name sortKey="Bogatcheva, Natalia V" sort="Bogatcheva, Natalia V" uniqKey="Bogatcheva N" first="Natalia V" last="Bogatcheva">Natalia V. Bogatcheva</name><name sortKey="Chelvanambi, Sarvesh" sort="Chelvanambi, Sarvesh" uniqKey="Chelvanambi S" first="Sarvesh" last="Chelvanambi">Sarvesh Chelvanambi</name><name sortKey="Clauss, Matthias" sort="Clauss, Matthias" uniqKey="Clauss M" first="Matthias" last="Clauss">Matthias Clauss</name><name sortKey="March, Keith L" sort="March, Keith L" uniqKey="March K" first="Keith L" last="March">Keith L. March</name><name sortKey="Poirier, Christophe" sort="Poirier, Christophe" uniqKey="Poirier C" first="Christophe" last="Poirier">Christophe Poirier</name><name sortKey="Saliba, Jacob" sort="Saliba, Jacob" uniqKey="Saliba J" first="Jacob" last="Saliba">Jacob Saliba</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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