Elucidating the molecular physiopathology of acute respiratory distress syndrome in severe acute respiratory syndrome patients.
Identifieur interne : 001857 ( PubMed/Corpus ); précédent : 001856; suivant : 001858Elucidating the molecular physiopathology of acute respiratory distress syndrome in severe acute respiratory syndrome patients.
Auteurs : Say Li Kong ; Paul Chui ; Bing Lim ; Manuel Salto-TellezSource :
- Virus research [ 1872-7492 ] ; 2009.
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.
DOI: 10.1016/j.virusres.2009.07.014
PubMed: 19635508
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pubmed:19635508Le document en format XML
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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.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19635508</PMID><DateCompleted><Year>2009</Year><Month>11</Month><Day>23</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>07</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-7492</ISSN><JournalIssue CitedMedium="Internet"><Volume>145</Volume><Issue>2</Issue><PubDate><Year>2009</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Virus research</Title><ISOAbbreviation>Virus Res.</ISOAbbreviation></Journal><ArticleTitle>Elucidating the molecular physiopathology of acute respiratory distress syndrome in severe acute respiratory syndrome patients.</ArticleTitle><Pagination><MedlinePgn>260-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.virusres.2009.07.014</ELocationID><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kong</LastName><ForeName>Say Li</ForeName><Initials>SL</Initials><AffiliationInfo><Affiliation>Genome Institute of Singapore, A*STAR (Agency for Science, Technology and Research), 60 Biopolis Street, Genome, #02-01, Singapore 138672, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chui</LastName><ForeName>Paul</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Lim</LastName><ForeName>Bing</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Salto-Tellez</LastName><ForeName>Manuel</ForeName><Initials>M</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. 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IdType="doi">10.1016/j.virusres.2009.07.014</ArticleId><ArticleId IdType="pmc">PMC7114434</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>N Engl J Med. 2003 May 15;348(20):1953-66</Citation><ArticleIdList><ArticleId IdType="pubmed">12690092</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Curr Opin Immunol. 2006 Feb;18(1):3-9</Citation><ArticleIdList><ArticleId IdType="pubmed">16343886</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Immunol. 2002 Jun 1;168(11):5690-8</Citation><ArticleIdList><ArticleId IdType="pubmed">12023368</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Biol Chem. 1990 Sep 5;265(25):15049-57</Citation><ArticleIdList><ArticleId IdType="pubmed">2118520</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Arthritis Rheum. 2000 Mar;43(3):628-37</Citation><ArticleIdList><ArticleId IdType="pubmed">10728757</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Pediatrics. 2004 Jan;113(1 Pt 1):e7-14</Citation><ArticleIdList><ArticleId IdType="pubmed">14702488</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Pathol. 2004 Jun;203(2):622-30</Citation><ArticleIdList><ArticleId IdType="pubmed">15141376</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Nat Rev Mol Cell Biol. 2002 Sep;3(9):651-62</Citation><ArticleIdList><ArticleId IdType="pubmed">12209125</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Eur Respir J. 1999 May;13(5):1029-36</Citation><ArticleIdList><ArticleId IdType="pubmed">10414400</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Hepatology. 1997 Jul;26(1):98-106</Citation><ArticleIdList><ArticleId IdType="pubmed">9214457</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Med Res Rev. 2006 Jan;26(1):88-130</Citation><ArticleIdList><ArticleId IdType="pubmed">16216010</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>BMC Cancer. 2005 Sep 21;5:121</Citation><ArticleIdList><ArticleId IdType="pubmed">16176582</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Infect Immun. 2006 Aug;74(8):4708-14</Citation><ArticleIdList><ArticleId IdType="pubmed">16861658</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Immunol. 2004 Sep 15;173(6):4030-9</Citation><ArticleIdList><ArticleId IdType="pubmed">15356152</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Proc Natl Acad Sci U S A. 1996 Oct 29;93(22):12456-60</Citation><ArticleIdList><ArticleId IdType="pubmed">8901603</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Int J Infect Dis. 2004 Jul;8(4):217-22</Citation><ArticleIdList><ArticleId IdType="pubmed">15234325</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Nature. 2003 Nov 27;426(6965):450-4</Citation><ArticleIdList><ArticleId IdType="pubmed">14647384</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Am J Respir Crit Care Med. 1995 May;151(5):1576-81</Citation><ArticleIdList><ArticleId IdType="pubmed">7735617</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Surg Res. 2006 Jun 1;133(1):22-8</Citation><ArticleIdList><ArticleId IdType="pubmed">16690368</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Biol Chem. 2002 Oct 18;277(42):39899-908</Citation><ArticleIdList><ArticleId IdType="pubmed">12140290</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Pathol. 2004 Feb;202(2):145-56</Citation><ArticleIdList><ArticleId IdType="pubmed">14743496</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Immunol. 2006 Jun 15;176(12):7462-70</Citation><ArticleIdList><ArticleId IdType="pubmed">16751392</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Regul Pept. 2005 Jan 15;124(1-3):195-201</Citation><ArticleIdList><ArticleId IdType="pubmed">15544859</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Leukoc Biol. 1998 Jul;64(1):14-8</Citation><ArticleIdList><ArticleId IdType="pubmed">9665269</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>PLoS Pathog. 2007 Aug 10;3(8):e112</Citation><ArticleIdList><ArticleId IdType="pubmed">17696609</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>J Biol Chem. 2002 Oct 11;277(41):38205-11</Citation><ArticleIdList><ArticleId IdType="pubmed">12149254</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Cytokine. 2005 Jan 21;29(2):92-4</Citation><ArticleIdList><ArticleId IdType="pubmed">15598444</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Science. 1982 Feb 5;215(4533):691-3</Citation><ArticleIdList><ArticleId IdType="pubmed">7036344</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>Eur J Pharmacol. 2001 Dec 21;433(2-3):199-207</Citation><ArticleIdList><ArticleId IdType="pubmed">11755153</ArticleId></ArticleIdList></Reference></ReferenceList><ReferenceList><Reference><Citation>BMC Immunol. 2005 Jan 18;6:2</Citation><ArticleIdList><ArticleId 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