Protective effects of long pentraxin PTX3 on lung injury in a severe acute respiratory syndrome model in mice.
Identifieur interne : 001343 ( PubMed/Curation ); précédent : 001342; suivant : 001344Protective effects of long pentraxin PTX3 on lung injury in a severe acute respiratory syndrome model in mice.
Auteurs : Bing Han [Canada] ; Xuezhong Ma ; Jianhua Zhang ; Yu Zhang ; Xiaohui Bai ; David M. Hwang ; Shaf Keshavjee ; Gary A. Levy ; Ian Mcgilvray ; Mingyao LiuSource :
- Laboratory investigation; a journal of technical methods and pathology [ 1530-0307 ] ; 2012.
Descripteurs français
- KwdFr :
- Animaux, Charge virale, Modèles animaux de maladie humaine, Protéine C-réactive (génétique), Protéine C-réactive (physiologie), Protéines de tissu nerveux (génétique), Protéines de tissu nerveux (physiologie), Souris, Souris knockout, Syndrome respiratoire aigu sévère (), Syndrome respiratoire aigu sévère (virologie), Test ELISA.
- MESH :
- génétique : Protéine C-réactive, Protéines de tissu nerveux.
- physiologie : Protéine C-réactive, Protéines de tissu nerveux.
- virologie : Syndrome respiratoire aigu sévère.
- Animaux, Charge virale, Modèles animaux de maladie humaine, Souris, Souris knockout, Syndrome respiratoire aigu sévère, Test ELISA.
English descriptors
- KwdEn :
- Animals, C-Reactive Protein (genetics), C-Reactive Protein (physiology), Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Mice, Mice, Knockout, Nerve Tissue Proteins (genetics), Nerve Tissue Proteins (physiology), Severe Acute Respiratory Syndrome (prevention & control), Severe Acute Respiratory Syndrome (virology), Viral Load.
- MESH :
- chemical , genetics : C-Reactive Protein, Nerve Tissue Proteins.
- chemical , physiology : C-Reactive Protein, Nerve Tissue Proteins.
- prevention & control : Severe Acute Respiratory Syndrome.
- virology : Severe Acute Respiratory Syndrome.
- Animals, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Mice, Mice, Knockout, Viral Load.
Abstract
The outbreak of severe acute respiratory syndrome (SARS) in 2003 reinforces the potential of lethal pandemics of respiratory viral infections. The underlying mechanisms of SARS are still largely undefined. Long pentraxin PTX3, a humoral mediator of innate immunity, has been reported to have anti-viral effects. We examined the role of PTX3 in coronavirus murine hepatitis virus strain 1 (MHV-1)-induced acute lung injury, a previously reported animal model for SARS. PTX3-deficient mice (129/SvEv/C57BL6/J) and their wild-type (WT) littermates were intranasally infected MHV-1. These mice were also treated with recombinant PTX3. Effects of PTX3 on viral binding and infectivity were determined in vitro. Cytokine expression, severity of lung injury, leukocyte infiltration and inflammatory responses were examined in vivo. In PTX3 WT mice, MHV-1 induced PTX3 expression in the lung and serum in a time-dependent manner. MHV-1 infection led to acute lung injury with greater severity in PTX3-deficient mice than that in WT mice. PTX3 deficiency enhanced early infiltration of neutrophils and macrophages in the lung. PTX3 bound to MHV-1 and MHV-3 and reduced MHV-1 infectivity in vitro. Administration of recombinant PTX3 significantly accelerated viral clearance in the lung, attenuated MHV-1-induced lung injury, and reduced early neutrophil influx and elevation of inflammatory mediators in the lung. Results from this study indicate a protective role of PTX3 in coronaviral infection-induced acute lung injury.
DOI: 10.1038/labinvest.2012.92
PubMed: 22732935
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Levy</name></author><author><name sortKey="Mcgilvray, Ian" sort="Mcgilvray, Ian" uniqKey="Mcgilvray I" first="Ian" last="Mcgilvray">Ian Mcgilvray</name></author><author><name sortKey="Liu, Mingyao" sort="Liu, Mingyao" uniqKey="Liu M" first="Mingyao" last="Liu">Mingyao Liu</name></author></analytic><series><title level="j">Laboratory investigation; a journal of technical methods and pathology</title><idno type="eISSN">1530-0307</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>C-Reactive Protein (genetics)</term><term>C-Reactive Protein (physiology)</term><term>Disease Models, Animal</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Mice</term><term>Mice, Knockout</term><term>Nerve Tissue Proteins (genetics)</term><term>Nerve Tissue Proteins (physiology)</term><term>Severe Acute Respiratory Syndrome (prevention & control)</term><term>Severe Acute Respiratory Syndrome (virology)</term><term>Viral Load</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Charge virale</term><term>Modèles animaux de maladie humaine</term><term>Protéine C-réactive (génétique)</term><term>Protéine C-réactive (physiologie)</term><term>Protéines de tissu nerveux (génétique)</term><term>Protéines de tissu nerveux (physiologie)</term><term>Souris</term><term>Souris knockout</term><term>Syndrome respiratoire aigu sévère ()</term><term>Syndrome respiratoire aigu sévère (virologie)</term><term>Test ELISA</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>C-Reactive Protein</term><term>Nerve Tissue Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>C-Reactive Protein</term><term>Nerve Tissue Proteins</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Protéine C-réactive</term><term>Protéines de tissu nerveux</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Protéine C-réactive</term><term>Protéines de tissu nerveux</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Mice</term><term>Mice, Knockout</term><term>Viral Load</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Charge virale</term><term>Modèles animaux de maladie humaine</term><term>Souris</term><term>Souris knockout</term><term>Syndrome respiratoire aigu sévère</term><term>Test ELISA</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The outbreak of severe acute respiratory syndrome (SARS) in 2003 reinforces the potential of lethal pandemics of respiratory viral infections. The underlying mechanisms of SARS are still largely undefined. Long pentraxin PTX3, a humoral mediator of innate immunity, has been reported to have anti-viral effects. We examined the role of PTX3 in coronavirus murine hepatitis virus strain 1 (MHV-1)-induced acute lung injury, a previously reported animal model for SARS. PTX3-deficient mice (129/SvEv/C57BL6/J) and their wild-type (WT) littermates were intranasally infected MHV-1. These mice were also treated with recombinant PTX3. Effects of PTX3 on viral binding and infectivity were determined in vitro. Cytokine expression, severity of lung injury, leukocyte infiltration and inflammatory responses were examined in vivo. In PTX3 WT mice, MHV-1 induced PTX3 expression in the lung and serum in a time-dependent manner. MHV-1 infection led to acute lung injury with greater severity in PTX3-deficient mice than that in WT mice. PTX3 deficiency enhanced early infiltration of neutrophils and macrophages in the lung. PTX3 bound to MHV-1 and MHV-3 and reduced MHV-1 infectivity in vitro. Administration of recombinant PTX3 significantly accelerated viral clearance in the lung, attenuated MHV-1-induced lung injury, and reduced early neutrophil influx and elevation of inflammatory mediators in the lung. Results from this study indicate a protective role of PTX3 in coronaviral infection-induced acute lung injury.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22732935</PMID><DateCompleted><Year>2012</Year><Month>11</Month><Day>08</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1530-0307</ISSN><JournalIssue CitedMedium="Internet"><Volume>92</Volume><Issue>9</Issue><PubDate><Year>2012</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Laboratory investigation; a journal of technical methods and pathology</Title><ISOAbbreviation>Lab. Invest.</ISOAbbreviation></Journal><ArticleTitle>Protective effects of long pentraxin PTX3 on lung injury in a severe acute respiratory syndrome model in mice.</ArticleTitle><Pagination><MedlinePgn>1285-96</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/labinvest.2012.92</ELocationID><Abstract><AbstractText>The outbreak of severe acute respiratory syndrome (SARS) in 2003 reinforces the potential of lethal pandemics of respiratory viral infections. The underlying mechanisms of SARS are still largely undefined. Long pentraxin PTX3, a humoral mediator of innate immunity, has been reported to have anti-viral effects. We examined the role of PTX3 in coronavirus murine hepatitis virus strain 1 (MHV-1)-induced acute lung injury, a previously reported animal model for SARS. PTX3-deficient mice (129/SvEv/C57BL6/J) and their wild-type (WT) littermates were intranasally infected MHV-1. These mice were also treated with recombinant PTX3. Effects of PTX3 on viral binding and infectivity were determined in vitro. Cytokine expression, severity of lung injury, leukocyte infiltration and inflammatory responses were examined in vivo. In PTX3 WT mice, MHV-1 induced PTX3 expression in the lung and serum in a time-dependent manner. MHV-1 infection led to acute lung injury with greater severity in PTX3-deficient mice than that in WT mice. PTX3 deficiency enhanced early infiltration of neutrophils and macrophages in the lung. PTX3 bound to MHV-1 and MHV-3 and reduced MHV-1 infectivity in vitro. Administration of recombinant PTX3 significantly accelerated viral clearance in the lung, attenuated MHV-1-induced lung injury, and reduced early neutrophil influx and elevation of inflammatory mediators in the lung. Results from this study indicate a protective role of PTX3 in coronaviral infection-induced acute lung injury.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Han</LastName><ForeName>Bing</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Latner Thoracic Surgery Research Laboratories, University Health Network Toronto General Hospital, Toronto, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ma</LastName><ForeName>Xuezhong</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Jianhua</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Yu</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Bai</LastName><ForeName>Xiaohui</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Hwang</LastName><ForeName>David M</ForeName><Initials>DM</Initials></Author><Author ValidYN="Y"><LastName>Keshavjee</LastName><ForeName>Shaf</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Levy</LastName><ForeName>Gary A</ForeName><Initials>GA</Initials></Author><Author ValidYN="Y"><LastName>McGilvray</LastName><ForeName>Ian</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Mingyao</ForeName><Initials>M</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>13270-4</GrantID><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant><Grant><GrantID>MOP-13270</GrantID><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant><Grant><GrantID>MOP-42546</GrantID><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. 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