Altered p38 mitogen-activated protein kinase expression in different leukocytes with increment of immunosuppressive mediators in patients with severe acute respiratory syndrome.
Identifieur interne : 002E45 ( PubMed/Checkpoint ); précédent : 002E44; suivant : 002E46Altered p38 mitogen-activated protein kinase expression in different leukocytes with increment of immunosuppressive mediators in patients with severe acute respiratory syndrome.
Auteurs : Chen-Hsiang Lee [Taïwan] ; Rong-Fu Chen ; Jien-Wei Liu ; Wen-Tien Yeh ; Jen-Chieh Chang ; Po-Mai Liu ; Hock-Liew Eng ; Meng-Chih Lin ; Kuender D. YangSource :
- Journal of immunology (Baltimore, Md. : 1950) [ 0022-1767 ] ; 2004.
Descripteurs français
- KwdFr :
- Adjuvants immunologiques (sang), Adulte, Adulte d'âge moyen, Charge virale, Coronavirus, Cytokines (sang), Dinoprostone (biosynthèse), Facteur de croissance transformant bêta (biosynthèse), Flambées de maladies, Humains, Leucocytes (enzymologie), Leucocytes (virologie), Mitogen-Activated Protein Kinases (analyse), Mitogen-Activated Protein Kinases (biosynthèse), Nitrates (sang), Régulation de l'expression des gènes codant pour des enzymes, Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (sang), Syndrome respiratoire aigu sévère (étiologie), p38 Mitogen-Activated Protein Kinases, Études cas-témoins.
- MESH :
- analyse : Mitogen-Activated Protein Kinases.
- biosynthèse : Dinoprostone, Facteur de croissance transformant bêta, Mitogen-Activated Protein Kinases.
- enzymologie : Leucocytes.
- immunologie : Syndrome respiratoire aigu sévère.
- sang : Adjuvants immunologiques, Cytokines, Nitrates, Syndrome respiratoire aigu sévère.
- virologie : Leucocytes.
- étiologie : Syndrome respiratoire aigu sévère.
- Adulte, Adulte d'âge moyen, Charge virale, Coronavirus, Flambées de maladies, Humains, Régulation de l'expression des gènes codant pour des enzymes, p38 Mitogen-Activated Protein Kinases, Études cas-témoins.
English descriptors
- KwdEn :
- Adjuvants, Immunologic (blood), Adult, Case-Control Studies, Coronavirus, Cytokines (blood), Dinoprostone (biosynthesis), Disease Outbreaks, Gene Expression Regulation, Enzymologic, Humans, Leukocytes (enzymology), Leukocytes (virology), Middle Aged, Mitogen-Activated Protein Kinases (analysis), Mitogen-Activated Protein Kinases (biosynthesis), Nitrates (blood), Severe Acute Respiratory Syndrome (blood), Severe Acute Respiratory Syndrome (etiology), Severe Acute Respiratory Syndrome (immunology), Transforming Growth Factor beta (biosynthesis), Viral Load, p38 Mitogen-Activated Protein Kinases.
- MESH :
- chemical , analysis : Mitogen-Activated Protein Kinases.
- chemical , biosynthesis : Dinoprostone, Mitogen-Activated Protein Kinases, Transforming Growth Factor beta.
- chemical , blood : Adjuvants, Immunologic, Cytokines, Nitrates.
- blood : Severe Acute Respiratory Syndrome.
- enzymology : Leukocytes.
- etiology : Severe Acute Respiratory Syndrome.
- immunology : Severe Acute Respiratory Syndrome.
- virology : Leukocytes.
- Adult, Case-Control Studies, Coronavirus, Disease Outbreaks, Gene Expression Regulation, Enzymologic, Humans, Middle Aged, Viral Load, p38 Mitogen-Activated Protein Kinases.
Abstract
Severe acute respiratory syndrome (SARS) has spread to a global pandemic, especially in Asia. The transmission route of SARS has been clarified, but the immunopathogenesis of SARS is unclear. In an age-matched case-control design, we studied immune parameters in 15 SARS patients who were previously healthy. Plasma was harvested for detection of virus load, cytokines, and nitrite/nitrate levels, and blood leukocytes were subjected to flow cytometric analysis of intracellular mitogen-activated protein kinases (MAPKs) in different leukocytes. Patients with SARS had significantly higher IL-8 levels (p = 0.016) in early stage, and higher IL-2 levels (p = 0.039) in late stage than normal controls. Blood TNF-alpha, IL-6, and IL-10, and nitrite/nitrate levels were not significantly elevated. In contrast, TGF-beta and PGE(2) levels were significantly elevated in SARS patients. Five of the 15 SARS patients had detectable coronaviruses in blood, but patients with detectable and undetectable viremia had no different profiles of immune mediators. Flow cytometric analysis of MAPKs activation by phospho-p38 and phospho-p44/42 (extracellular signal-regulated kinase) expression showed that augmented p38 activation (p = 0.044) of CD14 monocytes associated with suppressed p38 activation (p = 0.033) of CD8 lymphocytes was found in SARS patients. These results suggest that regulation of TGF-beta and PGE(2) production and MAPKs activation in different leukocytes may be considered while developing therapeutics for the SARS treatment.
DOI: 10.4049/jimmunol.172.12.7841
PubMed: 15187168
Affiliations:
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Yang</name></author></analytic><series><title level="j">Journal of immunology (Baltimore, Md. : 1950)</title><idno type="ISSN">0022-1767</idno><imprint><date when="2004" type="published">2004</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adjuvants, Immunologic (blood)</term><term>Adult</term><term>Case-Control Studies</term><term>Coronavirus</term><term>Cytokines (blood)</term><term>Dinoprostone (biosynthesis)</term><term>Disease Outbreaks</term><term>Gene Expression Regulation, Enzymologic</term><term>Humans</term><term>Leukocytes (enzymology)</term><term>Leukocytes (virology)</term><term>Middle Aged</term><term>Mitogen-Activated Protein Kinases (analysis)</term><term>Mitogen-Activated Protein Kinases (biosynthesis)</term><term>Nitrates (blood)</term><term>Severe Acute Respiratory Syndrome (blood)</term><term>Severe Acute Respiratory Syndrome (etiology)</term><term>Severe Acute Respiratory Syndrome (immunology)</term><term>Transforming Growth Factor beta (biosynthesis)</term><term>Viral Load</term><term>p38 Mitogen-Activated Protein Kinases</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adjuvants immunologiques (sang)</term><term>Adulte</term><term>Adulte d'âge moyen</term><term>Charge virale</term><term>Coronavirus</term><term>Cytokines (sang)</term><term>Dinoprostone (biosynthèse)</term><term>Facteur de croissance transformant bêta (biosynthèse)</term><term>Flambées de maladies</term><term>Humains</term><term>Leucocytes (enzymologie)</term><term>Leucocytes (virologie)</term><term>Mitogen-Activated Protein Kinases (analyse)</term><term>Mitogen-Activated Protein Kinases (biosynthèse)</term><term>Nitrates (sang)</term><term>Régulation de l'expression des gènes codant pour des enzymes</term><term>Syndrome respiratoire aigu sévère (immunologie)</term><term>Syndrome respiratoire aigu sévère (sang)</term><term>Syndrome respiratoire aigu sévère (étiologie)</term><term>p38 Mitogen-Activated Protein Kinases</term><term>Études cas-témoins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Mitogen-Activated Protein Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Dinoprostone</term><term>Mitogen-Activated Protein Kinases</term><term>Transforming Growth Factor beta</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Adjuvants, Immunologic</term><term>Cytokines</term><term>Nitrates</term></keywords><keywords scheme="MESH" qualifier="analyse" xml:lang="fr"><term>Mitogen-Activated Protein Kinases</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Dinoprostone</term><term>Facteur de croissance transformant bêta</term><term>Mitogen-Activated Protein Kinases</term></keywords><keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Leucocytes</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Leukocytes</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="sang" xml:lang="fr"><term>Adjuvants immunologiques</term><term>Cytokines</term><term>Nitrates</term><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Leucocytes</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Leukocytes</term></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Case-Control Studies</term><term>Coronavirus</term><term>Disease Outbreaks</term><term>Gene Expression Regulation, Enzymologic</term><term>Humans</term><term>Middle Aged</term><term>Viral Load</term><term>p38 Mitogen-Activated Protein Kinases</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adulte</term><term>Adulte d'âge moyen</term><term>Charge virale</term><term>Coronavirus</term><term>Flambées de maladies</term><term>Humains</term><term>Régulation de l'expression des gènes codant pour des enzymes</term><term>p38 Mitogen-Activated Protein Kinases</term><term>Études cas-témoins</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS) has spread to a global pandemic, especially in Asia. The transmission route of SARS has been clarified, but the immunopathogenesis of SARS is unclear. In an age-matched case-control design, we studied immune parameters in 15 SARS patients who were previously healthy. Plasma was harvested for detection of virus load, cytokines, and nitrite/nitrate levels, and blood leukocytes were subjected to flow cytometric analysis of intracellular mitogen-activated protein kinases (MAPKs) in different leukocytes. Patients with SARS had significantly higher IL-8 levels (p = 0.016) in early stage, and higher IL-2 levels (p = 0.039) in late stage than normal controls. Blood TNF-alpha, IL-6, and IL-10, and nitrite/nitrate levels were not significantly elevated. In contrast, TGF-beta and PGE(2) levels were significantly elevated in SARS patients. Five of the 15 SARS patients had detectable coronaviruses in blood, but patients with detectable and undetectable viremia had no different profiles of immune mediators. Flow cytometric analysis of MAPKs activation by phospho-p38 and phospho-p44/42 (extracellular signal-regulated kinase) expression showed that augmented p38 activation (p = 0.044) of CD14 monocytes associated with suppressed p38 activation (p = 0.033) of CD8 lymphocytes was found in SARS patients. These results suggest that regulation of TGF-beta and PGE(2) production and MAPKs activation in different leukocytes may be considered while developing therapeutics for the SARS treatment.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15187168</PMID><DateCompleted><Year>2004</Year><Month>09</Month><Day>16</Day></DateCompleted><DateRevised><Year>2019</Year><Month>05</Month><Day>16</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-1767</ISSN><JournalIssue CitedMedium="Print"><Volume>172</Volume><Issue>12</Issue><PubDate><Year>2004</Year><Month>Jun</Month><Day>15</Day></PubDate></JournalIssue><Title>Journal of immunology (Baltimore, Md. : 1950)</Title><ISOAbbreviation>J. Immunol.</ISOAbbreviation></Journal><ArticleTitle>Altered p38 mitogen-activated protein kinase expression in different leukocytes with increment of immunosuppressive mediators in patients with severe acute respiratory syndrome.</ArticleTitle><Pagination><MedlinePgn>7841-7</MedlinePgn></Pagination><Abstract><AbstractText>Severe acute respiratory syndrome (SARS) has spread to a global pandemic, especially in Asia. The transmission route of SARS has been clarified, but the immunopathogenesis of SARS is unclear. In an age-matched case-control design, we studied immune parameters in 15 SARS patients who were previously healthy. Plasma was harvested for detection of virus load, cytokines, and nitrite/nitrate levels, and blood leukocytes were subjected to flow cytometric analysis of intracellular mitogen-activated protein kinases (MAPKs) in different leukocytes. Patients with SARS had significantly higher IL-8 levels (p = 0.016) in early stage, and higher IL-2 levels (p = 0.039) in late stage than normal controls. Blood TNF-alpha, IL-6, and IL-10, and nitrite/nitrate levels were not significantly elevated. In contrast, TGF-beta and PGE(2) levels were significantly elevated in SARS patients. Five of the 15 SARS patients had detectable coronaviruses in blood, but patients with detectable and undetectable viremia had no different profiles of immune mediators. Flow cytometric analysis of MAPKs activation by phospho-p38 and phospho-p44/42 (extracellular signal-regulated kinase) expression showed that augmented p38 activation (p = 0.044) of CD14 monocytes associated with suppressed p38 activation (p = 0.033) of CD8 lymphocytes was found in SARS patients. These results suggest that regulation of TGF-beta and PGE(2) production and MAPKs activation in different leukocytes may be considered while developing therapeutics for the SARS treatment.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Chen-Hsiang</ForeName><Initials>CH</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine, Chang Gung Memorial Hospital, 123 Ta-Pei Road, Niau-Sung, Kaohsiung 833, Taiwan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Rong-Fu</ForeName><Initials>RF</Initials></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Jien-Wei</ForeName><Initials>JW</Initials></Author><Author ValidYN="Y"><LastName>Yeh</LastName><ForeName>Wen-Tien</ForeName><Initials>WT</Initials></Author><Author ValidYN="Y"><LastName>Chang</LastName><ForeName>Jen-Chieh</ForeName><Initials>JC</Initials></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Po-Mai</ForeName><Initials>PM</Initials></Author><Author ValidYN="Y"><LastName>Eng</LastName><ForeName>Hock-Liew</ForeName><Initials>HL</Initials></Author><Author ValidYN="Y"><LastName>Lin</LastName><ForeName>Meng-Chih</ForeName><Initials>MC</Initials></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Kuender D</ForeName><Initials>KD</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><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>J Immunol</MedlineTA><NlmUniqueID>2985117R</NlmUniqueID><ISSNLinking>0022-1767</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000276">Adjuvants, Immunologic</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009566">Nitrates</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016212">Transforming Growth Factor beta</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber><NameOfSubstance UI="D020928">Mitogen-Activated Protein Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber><NameOfSubstance UI="D048051">p38 Mitogen-Activated Protein Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>K7Q1JQR04M</RegistryNumber><NameOfSubstance UI="D015232">Dinoprostone</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000276" MajorTopicYN="N">Adjuvants, Immunologic</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016022" MajorTopicYN="N">Case-Control Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017934" MajorTopicYN="N">Coronavirus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015232" MajorTopicYN="N">Dinoprostone</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004196" MajorTopicYN="N">Disease Outbreaks</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015971" MajorTopicYN="N">Gene Expression Regulation, Enzymologic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007962" MajorTopicYN="N">Leukocytes</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="Y">enzymology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020928" MajorTopicYN="N">Mitogen-Activated Protein Kinases</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000096" MajorTopicYN="Y">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009566" MajorTopicYN="N">Nitrates</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045169" MajorTopicYN="N">Severe Acute Respiratory Syndrome</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016212" MajorTopicYN="N">Transforming Growth Factor beta</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019562" MajorTopicYN="N">Viral Load</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D048051" MajorTopicYN="N">p38 Mitogen-Activated Protein Kinases</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2004</Year><Month>6</Month><Day>10</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2004</Year><Month>9</Month><Day>17</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2004</Year><Month>6</Month><Day>10</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">15187168</ArticleId><ArticleId IdType="pii">172/12/7841</ArticleId><ArticleId IdType="doi">10.4049/jimmunol.172.12.7841</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Taïwan</li></country></list><tree><noCountry><name sortKey="Chang, Jen Chieh" sort="Chang, Jen Chieh" uniqKey="Chang J" first="Jen-Chieh" last="Chang">Jen-Chieh Chang</name><name sortKey="Chen, Rong Fu" sort="Chen, Rong Fu" uniqKey="Chen R" first="Rong-Fu" last="Chen">Rong-Fu Chen</name><name sortKey="Eng, Hock Liew" sort="Eng, Hock Liew" uniqKey="Eng H" first="Hock-Liew" last="Eng">Hock-Liew Eng</name><name sortKey="Lin, Meng Chih" sort="Lin, Meng Chih" uniqKey="Lin M" first="Meng-Chih" last="Lin">Meng-Chih Lin</name><name sortKey="Liu, Jien Wei" sort="Liu, Jien Wei" uniqKey="Liu J" first="Jien-Wei" last="Liu">Jien-Wei Liu</name><name sortKey="Liu, Po Mai" sort="Liu, Po Mai" uniqKey="Liu P" first="Po-Mai" last="Liu">Po-Mai Liu</name><name sortKey="Yang, Kuender D" sort="Yang, Kuender D" uniqKey="Yang K" first="Kuender D" last="Yang">Kuender D. Yang</name><name sortKey="Yeh, Wen Tien" sort="Yeh, Wen Tien" uniqKey="Yeh W" first="Wen-Tien" last="Yeh">Wen-Tien Yeh</name></noCountry><country name="Taïwan"><noRegion><name sortKey="Lee, Chen Hsiang" sort="Lee, Chen Hsiang" uniqKey="Lee C" first="Chen-Hsiang" last="Lee">Chen-Hsiang Lee</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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