The spleen as a target in severe acute respiratory syndrome.
Identifieur interne : 002002 ( PubMed/Corpus ); précédent : 002001; suivant : 002003The spleen as a target in severe acute respiratory syndrome.
Auteurs : Jun Zhan ; Ruishu Deng ; Junmin Tang ; Bo Zhang ; Yan Tang ; Jeffrey K. Wang ; Feng Li ; Virginia M. Anderson ; Michael A. Mcnutt ; Jiang GuSource :
- FASEB journal : official publication of the Federation of American Societies for Experimental Biology [ 1530-6860 ] ; 2006.
English descriptors
- KwdEn :
- MESH :
- chemical , analysis : Antigens, CD.
- genetics : Coronavirus.
- isolation & purification : Coronavirus.
- pathology : Severe Acute Respiratory Syndrome, Spleen.
- Adult, Autopsy, Base Sequence, DNA Primers, Genome, Viral, Humans, In Situ Hybridization, Male, Middle Aged, Polymerase Chain Reaction.
Abstract
It has been proposed that immune injury is the central mechanism of pathogenesis of the infectious disease, severe acute respiratory syndrome (SARS). To gain a better understanding of immune injury in the spleen, we investigated the number and distribution of various immune cell types in the spleens of SARS patients. We performed autopsies on six confirmed SARS cases, with six normal subjects as controls; spleen samples from these autopsies were examined with hematoxylin and eosin (H&E) sections, in situ hybridization for SARS virus genomic sequences, and immunohistochemistry with seven monoclonal antibodies to five cell types. The number and distribution of these cells were measured and analyzed using an image analysis system. SARS genomic sequences were detected in all SARS spleens. The SARS spleens all had severe damage to the white pulp and showed an alteration of the normal distribution of various cell types. Immunocytes in the red pulp were decreased by 68.0-90.7% except for CD68+ macrophages and human leukocyte antigen (HLA)-DR positive antigen-presenting cells (APC), which were decreased to a lesser degree. On average, CD68+ macrophages were increased in size by 2.21-fold. We hypothesize that the collapse of the splenic immune system plays a key role in the clinical outcome of these patients.
DOI: 10.1096/fj.06-6324com
PubMed: 17077309
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pubmed:17077309Le document en format XML
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Wang</name></author><author><name sortKey="Li, Feng" sort="Li, Feng" uniqKey="Li F" first="Feng" last="Li">Feng Li</name></author><author><name sortKey="Anderson, Virginia M" sort="Anderson, Virginia M" uniqKey="Anderson V" first="Virginia M" last="Anderson">Virginia M. Anderson</name></author><author><name sortKey="Mcnutt, Michael A" sort="Mcnutt, Michael A" uniqKey="Mcnutt M" first="Michael A" last="Mcnutt">Michael A. Mcnutt</name></author><author><name sortKey="Gu, Jiang" sort="Gu, Jiang" uniqKey="Gu J" first="Jiang" last="Gu">Jiang Gu</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2006">2006</date><idno type="RBID">pubmed:17077309</idno><idno type="pmid">17077309</idno><idno type="doi">10.1096/fj.06-6324com</idno><idno type="wicri:Area/PubMed/Corpus">002002</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002002</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The spleen as a target in severe acute respiratory syndrome.</title><author><name sortKey="Zhan, Jun" sort="Zhan, Jun" uniqKey="Zhan J" first="Jun" last="Zhan">Jun Zhan</name><affiliation><nlm:affiliation>Department of Histology and Embryology, Peking University Health Science Center, Beijing, China.</nlm:affiliation></affiliation></author><author><name sortKey="Deng, Ruishu" sort="Deng, Ruishu" uniqKey="Deng R" first="Ruishu" last="Deng">Ruishu Deng</name></author><author><name sortKey="Tang, Junmin" sort="Tang, Junmin" uniqKey="Tang J" first="Junmin" last="Tang">Junmin Tang</name></author><author><name sortKey="Zhang, Bo" sort="Zhang, Bo" uniqKey="Zhang B" first="Bo" last="Zhang">Bo Zhang</name></author><author><name sortKey="Tang, Yan" sort="Tang, Yan" uniqKey="Tang Y" first="Yan" last="Tang">Yan Tang</name></author><author><name sortKey="Wang, Jeffrey K" sort="Wang, Jeffrey K" uniqKey="Wang J" first="Jeffrey K" last="Wang">Jeffrey K. Wang</name></author><author><name sortKey="Li, Feng" sort="Li, Feng" uniqKey="Li F" first="Feng" last="Li">Feng Li</name></author><author><name sortKey="Anderson, Virginia M" sort="Anderson, Virginia M" uniqKey="Anderson V" first="Virginia M" last="Anderson">Virginia M. Anderson</name></author><author><name sortKey="Mcnutt, Michael A" sort="Mcnutt, Michael A" uniqKey="Mcnutt M" first="Michael A" last="Mcnutt">Michael A. Mcnutt</name></author><author><name sortKey="Gu, Jiang" sort="Gu, Jiang" uniqKey="Gu J" first="Jiang" last="Gu">Jiang Gu</name></author></analytic><series><title level="j">FASEB journal : official publication of the Federation of American Societies for Experimental Biology</title><idno type="eISSN">1530-6860</idno><imprint><date when="2006" type="published">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Antigens, CD (analysis)</term><term>Autopsy</term><term>Base Sequence</term><term>Coronavirus (genetics)</term><term>Coronavirus (isolation & purification)</term><term>DNA Primers</term><term>Genome, Viral</term><term>Humans</term><term>In Situ Hybridization</term><term>Male</term><term>Middle Aged</term><term>Polymerase Chain Reaction</term><term>Severe Acute Respiratory Syndrome (pathology)</term><term>Spleen (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Antigens, CD</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Coronavirus</term></keywords><keywords scheme="MESH" qualifier="isolation & purification" xml:lang="en"><term>Coronavirus</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term><term>Spleen</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Autopsy</term><term>Base Sequence</term><term>DNA Primers</term><term>Genome, Viral</term><term>Humans</term><term>In Situ Hybridization</term><term>Male</term><term>Middle Aged</term><term>Polymerase Chain Reaction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">It has been proposed that immune injury is the central mechanism of pathogenesis of the infectious disease, severe acute respiratory syndrome (SARS). To gain a better understanding of immune injury in the spleen, we investigated the number and distribution of various immune cell types in the spleens of SARS patients. We performed autopsies on six confirmed SARS cases, with six normal subjects as controls; spleen samples from these autopsies were examined with hematoxylin and eosin (H&E) sections, in situ hybridization for SARS virus genomic sequences, and immunohistochemistry with seven monoclonal antibodies to five cell types. The number and distribution of these cells were measured and analyzed using an image analysis system. SARS genomic sequences were detected in all SARS spleens. The SARS spleens all had severe damage to the white pulp and showed an alteration of the normal distribution of various cell types. Immunocytes in the red pulp were decreased by 68.0-90.7% except for CD68+ macrophages and human leukocyte antigen (HLA)-DR positive antigen-presenting cells (APC), which were decreased to a lesser degree. On average, CD68+ macrophages were increased in size by 2.21-fold. We hypothesize that the collapse of the splenic immune system plays a key role in the clinical outcome of these patients.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17077309</PMID><DateCompleted><Year>2006</Year><Month>11</Month><Day>27</Day></DateCompleted><DateRevised><Year>2012</Year><Month>02</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1530-6860</ISSN><JournalIssue CitedMedium="Internet"><Volume>20</Volume><Issue>13</Issue><PubDate><Year>2006</Year><Month>Nov</Month></PubDate></JournalIssue><Title>FASEB journal : official publication of the Federation of American Societies for Experimental Biology</Title><ISOAbbreviation>FASEB J.</ISOAbbreviation></Journal><ArticleTitle>The spleen as a target in severe acute respiratory syndrome.</ArticleTitle><Pagination><MedlinePgn>2321-8</MedlinePgn></Pagination><Abstract><AbstractText>It has been proposed that immune injury is the central mechanism of pathogenesis of the infectious disease, severe acute respiratory syndrome (SARS). To gain a better understanding of immune injury in the spleen, we investigated the number and distribution of various immune cell types in the spleens of SARS patients. We performed autopsies on six confirmed SARS cases, with six normal subjects as controls; spleen samples from these autopsies were examined with hematoxylin and eosin (H&E) sections, in situ hybridization for SARS virus genomic sequences, and immunohistochemistry with seven monoclonal antibodies to five cell types. The number and distribution of these cells were measured and analyzed using an image analysis system. SARS genomic sequences were detected in all SARS spleens. The SARS spleens all had severe damage to the white pulp and showed an alteration of the normal distribution of various cell types. Immunocytes in the red pulp were decreased by 68.0-90.7% except for CD68+ macrophages and human leukocyte antigen (HLA)-DR positive antigen-presenting cells (APC), which were decreased to a lesser degree. On average, CD68+ macrophages were increased in size by 2.21-fold. We hypothesize that the collapse of the splenic immune system plays a key role in the clinical outcome of these patients.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhan</LastName><ForeName>Jun</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Histology and Embryology, Peking University Health Science Center, Beijing, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Deng</LastName><ForeName>Ruishu</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Tang</LastName><ForeName>Junmin</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Bo</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Tang</LastName><ForeName>Yan</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Jeffrey K</ForeName><Initials>JK</Initials></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Feng</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Anderson</LastName><ForeName>Virginia M</ForeName><Initials>VM</Initials></Author><Author ValidYN="Y"><LastName>McNutt</LastName><ForeName>Michael A</ForeName><Initials>MA</Initials></Author><Author ValidYN="Y"><LastName>Gu</LastName><ForeName>Jiang</ForeName><Initials>J</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>FASEB J</MedlineTA><NlmUniqueID>8804484</NlmUniqueID><ISSNLinking>0892-6638</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015703">Antigens, CD</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017931">DNA Primers</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015703" MajorTopicYN="N">Antigens, CD</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001344" MajorTopicYN="N">Autopsy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001483" MajorTopicYN="N">Base Sequence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017934" MajorTopicYN="N">Coronavirus</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000302" MajorTopicYN="N">isolation & purification</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017931" MajorTopicYN="N">DNA Primers</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016679" MajorTopicYN="N">Genome, Viral</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017403" MajorTopicYN="N">In Situ Hybridization</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016133" MajorTopicYN="N">Polymerase Chain Reaction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D045169" MajorTopicYN="N">Severe Acute Respiratory Syndrome</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013154" MajorTopicYN="N">Spleen</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>11</Month><Day>2</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>12</Month><Day>9</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>11</Month><Day>2</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17077309</ArticleId><ArticleId IdType="pii">20/13/2321</ArticleId><ArticleId IdType="doi">10.1096/fj.06-6324com</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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