Elucidating the molecular physiopathology of acute respiratory distress syndrome in severe acute respiratory syndrome patients
Identifieur interne : 001F71 ( Ncbi/Checkpoint ); précédent : 001F70; suivant : 001F72Elucidating the molecular physiopathology of acute respiratory distress syndrome in severe acute respiratory syndrome patients
Auteurs : Say Li Kong [Singapour] ; Paul Chui [Singapour] ; Bing Lim [Singapour, États-Unis] ; Manuel Salto-Tellez [Singapour]Source :
- Virus Research [ 0168-1702 ] ; 2009.
Descripteurs français
- KwdFr :
- MESH :
English descriptors
- KwdEn :
- MESH :
- complications : Severe Acute Respiratory Syndrome.
- pathology : Lung, Respiratory Distress Syndrome, Adult.
- Adult, Aged, Autopsy, Female, Gene Expression Profiling, Humans, Immunohistochemistry, Male, Middle Aged, Severity of Illness Index.
Abstract
Acute respiratory distress syndrome (ARDS) is a severe form of acute lung injury. It is a response to various diseases of variable etiology, including SARS-CoV infection. To date, a comprehensive study of the genomic physiopathology of ARDS (and SARS) is lacking, primarily due to the difficulty of finding suitable materials to study the disease process at a tissue level (instead of blood, sputa or swaps). Hereby we attempt to provide such study by analyzing autopsy lung samples from patient who died of SARS and showed different degrees of severity of the pulmonary involvement. We performed real-time quantitative PCR analysis of 107 genes with functional roles in inflammation, coagulation, fibrosis and apoptosis; some key genes were confirmed at a protein expression level by immunohistochemistry and correlated to the degree of morphological severity present in the individual samples analyzed. Significant expression levels were identified for ANPEP (a receptor for CoV), as well as inhibition of the STAT1 pathway, IFNs production and CXCL10 (a T-cell recruiter). Other genes unassociated to date with ARDS/SARS include C1Qb, C5R1, CASP3, CASP9, CD14, CD68, FGF7, HLA-DRA, IGF1, IRF3, MALAT-1, MSR1, NFIL3, SLPI, USP33, CLC, GBP1 and TAC1. As a result, we proposed to therapeutically target some of these genes with compounds such as ANPEP inhibitors, SLPI and dexamethasone. Ultimately, this study may serve as a model for future, tissue-based analyses of fibroinflammatory conditions affecting the lung.
Url:
DOI: 10.1016/j.virusres.2009.07.014
PubMed: 19635508
PubMed Central: 7114434
Affiliations:
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Singapore</nlm:aff><country xml:lang="fr">Singapour</country><wicri:regionArea>Genome Institute of Singapore, A*STAR (Agency for Science, Technology and Research), 60 Biopolis Street, Genome, #02-01, Singapore 138672</wicri:regionArea><wicri:noRegion>Singapore 138672</wicri:noRegion></affiliation><affiliation wicri:level="2"><nlm:aff id="aff3">Harvard Institute of Medicine, 77 Ave Louis Pasteur, Boston, MA 02115, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Harvard Institute of Medicine, 77 Ave Louis Pasteur, Boston, MA 02115</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Salto Tellez, Manuel" sort="Salto Tellez, Manuel" uniqKey="Salto Tellez M" first="Manuel" last="Salto-Tellez">Manuel Salto-Tellez</name><affiliation wicri:level="1"><nlm:aff id="aff4">National University Health System and National University of Singapore, 5 Lower Kent Ridge Road, Singapore 119074, Singapore</nlm:aff><country xml:lang="fr">Singapour</country><wicri:regionArea>National University Health System and National University of Singapore, 5 Lower Kent Ridge Road, Singapore 119074</wicri:regionArea><wicri:noRegion>Singapore 119074</wicri:noRegion></affiliation></author></analytic><series><title level="j">Virus Research</title><idno type="ISSN">0168-1702</idno><idno type="eISSN">1872-7492</idno><imprint><date when="2009">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Autopsy</term><term>Female</term><term>Gene Expression Profiling</term><term>Humans</term><term>Immunohistochemistry</term><term>Lung (pathology)</term><term>Male</term><term>Middle Aged</term><term>Respiratory Distress Syndrome, Adult (pathology)</term><term>Severe Acute Respiratory Syndrome (complications)</term><term>Severity of Illness Index</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adulte</term><term>Adulte d'âge moyen</term><term>Analyse de profil d'expression de gènes</term><term>Autopsie</term><term>Femelle</term><term>Humains</term><term>Immunohistochimie</term><term>Indice de gravité médicale</term><term>Mâle</term><term>Poumon (anatomopathologie)</term><term>Sujet âgé</term><term>Syndrome de détresse respiratoire de l'adulte (anatomopathologie)</term><term>Syndrome respiratoire aigu sévère ()</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Poumon</term><term>Syndrome de détresse respiratoire de l'adulte</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term><term>Respiratory Distress Syndrome, Adult</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Autopsy</term><term>Female</term><term>Gene Expression Profiling</term><term>Humans</term><term>Immunohistochemistry</term><term>Male</term><term>Middle Aged</term><term>Severity of Illness Index</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adulte</term><term>Adulte d'âge moyen</term><term>Analyse de profil d'expression de gènes</term><term>Autopsie</term><term>Femelle</term><term>Humains</term><term>Immunohistochimie</term><term>Indice de gravité médicale</term><term>Mâle</term><term>Sujet âgé</term><term>Syndrome respiratoire aigu sévère</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Acute respiratory distress syndrome (ARDS) is a severe form of acute lung injury. It is a response to various diseases of variable etiology, including SARS-CoV infection. To date, a comprehensive study of the genomic physiopathology of ARDS (and SARS) is lacking, primarily due to the difficulty of finding suitable materials to study the disease process at a tissue level (instead of blood, sputa or swaps). Hereby we attempt to provide such study by analyzing autopsy lung samples from patient who died of SARS and showed different degrees of severity of the pulmonary involvement. We performed real-time quantitative PCR analysis of 107 genes with functional roles in inflammation, coagulation, fibrosis and apoptosis; some key genes were confirmed at a protein expression level by immunohistochemistry and correlated to the degree of morphological severity present in the individual samples analyzed. Significant expression levels were identified for ANPEP (a receptor for CoV), as well as inhibition of the STAT1 pathway, IFNs production and CXCL10 (a T-cell recruiter). Other genes unassociated to date with ARDS/SARS include C1Qb, C5R1, CASP3, CASP9, CD14, CD68, FGF7, HLA-DRA, IGF1, IRF3, MALAT-1, MSR1, NFIL3, SLPI, USP33, CLC, GBP1 and TAC1. As a result, we proposed to therapeutically target some of these genes with compounds such as ANPEP inhibitors, SLPI and dexamethasone. Ultimately, this study may serve as a model for future, tissue-based analyses of fibroinflammatory conditions affecting the lung.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Aichele, D" uniqKey="Aichele D">D. Aichele</name></author><author><name sortKey="Schnare, M" uniqKey="Schnare M">M. Schnare</name></author><author><name sortKey="Saake, M" uniqKey="Saake M">M. Saake</name></author><author><name sortKey="Rollinghoff, M" uniqKey="Rollinghoff M">M. Rollinghoff</name></author><author><name sortKey="Gessner, A" uniqKey="Gessner A">A. 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Zlateva</name></author><author><name sortKey="Van Ranst, M" uniqKey="Van Ranst M">M. Van Ranst</name></author></analytic></biblStruct><biblStruct></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Singapour</li><li>États-Unis</li></country><region><li>Massachusetts</li></region></list><tree><country name="Singapour"><noRegion><name sortKey="Kong, Say Li" sort="Kong, Say Li" uniqKey="Kong S" first="Say Li" last="Kong">Say Li Kong</name></noRegion><name sortKey="Chui, Paul" sort="Chui, Paul" uniqKey="Chui P" first="Paul" last="Chui">Paul Chui</name><name sortKey="Lim, Bing" sort="Lim, Bing" uniqKey="Lim B" first="Bing" last="Lim">Bing Lim</name><name sortKey="Salto Tellez, Manuel" sort="Salto Tellez, Manuel" uniqKey="Salto Tellez M" first="Manuel" last="Salto-Tellez">Manuel Salto-Tellez</name></country><country name="États-Unis"><region name="Massachusetts"><name sortKey="Lim, Bing" sort="Lim, Bing" uniqKey="Lim B" first="Bing" last="Lim">Bing Lim</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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