Inflammation inhibitors were remarkably up‐regulated in plasma of severe acute respiratory syndrome patients at progressive phase
Identifieur interne : 000F32 ( Istex/Checkpoint ); précédent : 000F31; suivant : 000F33Inflammation inhibitors were remarkably up‐regulated in plasma of severe acute respiratory syndrome patients at progressive phase
Auteurs : Jia Wan [République populaire de Chine] ; Wei Sun [République populaire de Chine] ; Xiaohai Li [République populaire de Chine] ; Wantao Ying [République populaire de Chine] ; Jingquan Dai [République populaire de Chine] ; Xuezhang Kuai [République populaire de Chine] ; Handong Wei [République populaire de Chine] ; Xue Gao [République populaire de Chine] ; Yunping Zhu [République populaire de Chine] ; Ying Jiang [République populaire de Chine] ; Xiaohong Qian [République populaire de Chine] ; Fuchu He [République populaire de Chine]Source :
- PROTEOMICS [ 1615-9853 ] ; 2006-05.
English descriptors
- Teeft :
- Acid glycoprotein, Alpha chains, Amersham biosciences, Beijing institute, Bioscience, Convalescent, Convalescent group, Convalescent phase, Convalescent phases, Decyder software, Decyder software analysis, Different groups, Different ptms, Different spots, Different volume ratios, Dige, Dige images, Disease process, Disease progression, Equilibration buffer, Fetuin, Gmbh, High level, Human fetuin, Human plasma, Immune system, Important role, Individual samples, Inflammation, Inflammation control, Inflammatory response, Kgaa, Negative apps, Normal group, Normal levels, Normal plasma, Peptide, Plasma protein, Plasma proteins, Positive role, Progression, Progressive group, Progressive phase, Protein, Protein spots, Proteomics, Quantitione software, Radiation medicine, Relative levels, Respiratory syndrome, Results show, Room temperature, Same protein, Sample preparation, Santa cruz biotechnology, Sars, Sars patients, Sars progression, Semiquantitative analysis, Several proteins, Significant change, Software, Symptom onset, Transthyretin, Verlag, Verlag gmbh, Volume ratio, Weinheim, Weinheim proteomics, Western blot, Western blot analysis.
Abstract
Severe acute respiratory syndrome (SARS) is a severe infectious disease that has affected many countries and regions since 2002. A novel member of the coronavirus, SARS‐CoV, has been identified as the causative agent. However, the pathogenesis of SARS is still elusive. In this study, we used 2‐D DIGE and MS to analyze the protein profiles of plasma from SARS patients, in the search for proteomic alterations associated with the disease progression, which could provide some clues to the pathogenesis. To enrich the low‐abundance proteins in human plasma, two highly abundant proteins, albumin and IgG, were first removed. By comparing the plasma proteins of SARS patients with those of a normal control group, several proteins with a significant alteration were found. The up‐regulated proteins were identified as alpha‐1 acid glycoprotein, haptoglobin, alpha‐1 anti‐chymotrypsin and fetuin. The down‐regulated proteins were apolipoprotein A‐I, transferrin and transthyretin. Most of the proteins showed significant changes (up‐ or down‐regulated) in the progressive phase of disease, and there was a trend back to normal level during the convalescent phase. Among these proteins, the alterations of fetuin and anti‐chymotrypsin were further confirmed by Western blotting. Since all the up‐regulated proteins identified above are well‐known inflammation inhibitors, these results strongly suggest that the body starts inflammation inhibition to sustain the inflammatory response balance in the progression of SARS.
Url:
DOI: 10.1002/pmic.200500638
Affiliations:
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and Proteomics, Beijing Institute of Radiation Medicine, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Wei, Handong" sort="Wei, Handong" uniqKey="Wei H" first="Handong" last="Wei">Handong Wei</name><affiliation wicri:level="3"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Genomics and Proteomics, Beijing Institute of Radiation Medicine, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Gao, Xue" sort="Gao, Xue" uniqKey="Gao X" first="Xue" last="Gao">Xue Gao</name><affiliation wicri:level="3"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Genomics and Proteomics, Beijing Institute of Radiation Medicine, Beijing</wicri:regionArea><placeName><settlement 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last="Qian">Xiaohong Qian</name><affiliation wicri:level="3"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Genomics and Proteomics, Beijing Institute of Radiation Medicine, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="He, Fuchu" sort="He, Fuchu" uniqKey="He F" first="Fuchu" last="He">Fuchu He</name><affiliation wicri:level="3"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Genomics and Proteomics, Beijing Institute of Radiation Medicine, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation><affiliation wicri:level="1"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institute of Biomedical Sciences Fudan University, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation><affiliation wicri:level="1"><country wicri:rule="url">République populaire de Chine</country></affiliation><affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">PROTEOMICS</title><title level="j" type="alt">PROTEOMICS</title><idno type="ISSN">1615-9853</idno><idno type="eISSN">1615-9861</idno><imprint><biblScope unit="vol">6</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="2886">2886</biblScope><biblScope unit="page" to="2894">2894</biblScope><biblScope unit="page-count">9</biblScope><publisher>WILEY‐VCH Verlag</publisher><pubPlace>Weinheim</pubPlace><date type="published" when="2006-05">2006-05</date></imprint><idno type="ISSN">1615-9853</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1615-9853</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Acid glycoprotein</term><term>Alpha chains</term><term>Amersham biosciences</term><term>Beijing institute</term><term>Bioscience</term><term>Convalescent</term><term>Convalescent group</term><term>Convalescent phase</term><term>Convalescent phases</term><term>Decyder software</term><term>Decyder software analysis</term><term>Different groups</term><term>Different ptms</term><term>Different spots</term><term>Different volume ratios</term><term>Dige</term><term>Dige images</term><term>Disease process</term><term>Disease progression</term><term>Equilibration buffer</term><term>Fetuin</term><term>Gmbh</term><term>High level</term><term>Human fetuin</term><term>Human plasma</term><term>Immune system</term><term>Important role</term><term>Individual samples</term><term>Inflammation</term><term>Inflammation control</term><term>Inflammatory response</term><term>Kgaa</term><term>Negative apps</term><term>Normal group</term><term>Normal levels</term><term>Normal plasma</term><term>Peptide</term><term>Plasma protein</term><term>Plasma proteins</term><term>Positive role</term><term>Progression</term><term>Progressive group</term><term>Progressive phase</term><term>Protein</term><term>Protein spots</term><term>Proteomics</term><term>Quantitione software</term><term>Radiation medicine</term><term>Relative levels</term><term>Respiratory syndrome</term><term>Results show</term><term>Room temperature</term><term>Same protein</term><term>Sample preparation</term><term>Santa cruz biotechnology</term><term>Sars</term><term>Sars patients</term><term>Sars progression</term><term>Semiquantitative analysis</term><term>Several proteins</term><term>Significant change</term><term>Software</term><term>Symptom onset</term><term>Transthyretin</term><term>Verlag</term><term>Verlag gmbh</term><term>Volume ratio</term><term>Weinheim</term><term>Weinheim proteomics</term><term>Western blot</term><term>Western blot analysis</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome (SARS) is a severe infectious disease that has affected many countries and regions since 2002. A novel member of the coronavirus, SARS‐CoV, has been identified as the causative agent. However, the pathogenesis of SARS is still elusive. In this study, we used 2‐D DIGE and MS to analyze the protein profiles of plasma from SARS patients, in the search for proteomic alterations associated with the disease progression, which could provide some clues to the pathogenesis. To enrich the low‐abundance proteins in human plasma, two highly abundant proteins, albumin and IgG, were first removed. By comparing the plasma proteins of SARS patients with those of a normal control group, several proteins with a significant alteration were found. The up‐regulated proteins were identified as alpha‐1 acid glycoprotein, haptoglobin, alpha‐1 anti‐chymotrypsin and fetuin. The down‐regulated proteins were apolipoprotein A‐I, transferrin and transthyretin. Most of the proteins showed significant changes (up‐ or down‐regulated) in the progressive phase of disease, and there was a trend back to normal level during the convalescent phase. Among these proteins, the alterations of fetuin and anti‐chymotrypsin were further confirmed by Western blotting. Since all the up‐regulated proteins identified above are well‐known inflammation inhibitors, these results strongly suggest that the body starts inflammation inhibition to sustain the inflammatory response balance in the progression of SARS.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country><settlement><li>Pékin</li></settlement></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Wan, Jia" sort="Wan, Jia" uniqKey="Wan J" first="Jia" last="Wan">Jia Wan</name></noRegion><name sortKey="Dai, Jingquan" sort="Dai, Jingquan" uniqKey="Dai J" first="Jingquan" last="Dai">Jingquan Dai</name><name sortKey="Gao, Xue" sort="Gao, Xue" uniqKey="Gao X" first="Xue" last="Gao">Xue Gao</name><name sortKey="He, Fuchu" sort="He, Fuchu" uniqKey="He F" first="Fuchu" last="He">Fuchu He</name><name sortKey="He, Fuchu" sort="He, Fuchu" uniqKey="He F" first="Fuchu" last="He">Fuchu He</name><name sortKey="He, Fuchu" sort="He, Fuchu" uniqKey="He F" first="Fuchu" last="He">Fuchu He</name><name sortKey="Jiang, Ying" sort="Jiang, Ying" uniqKey="Jiang Y" first="Ying" last="Jiang">Ying Jiang</name><name sortKey="Kuai, Xuezhang" sort="Kuai, Xuezhang" uniqKey="Kuai X" first="Xuezhang" last="Kuai">Xuezhang Kuai</name><name sortKey="Li, Xiaohai" sort="Li, Xiaohai" uniqKey="Li X" first="Xiaohai" last="Li">Xiaohai Li</name><name sortKey="Qian, Xiaohong" sort="Qian, Xiaohong" uniqKey="Qian X" first="Xiaohong" last="Qian">Xiaohong Qian</name><name sortKey="Sun, Wei" sort="Sun, Wei" uniqKey="Sun W" first="Wei" last="Sun">Wei Sun</name><name sortKey="Wei, Handong" sort="Wei, Handong" uniqKey="Wei H" first="Handong" last="Wei">Handong Wei</name><name sortKey="Ying, Wantao" sort="Ying, Wantao" uniqKey="Ying W" first="Wantao" last="Ying">Wantao Ying</name><name sortKey="Zhu, Yunping" sort="Zhu, Yunping" uniqKey="Zhu Y" first="Yunping" last="Zhu">Yunping Zhu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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