Characterization of cytokine/chemokine profiles of severe acute respiratory syndrome
Identifieur interne : 004E63 ( Main/Exploration ); précédent : 004E62; suivant : 004E64Characterization of cytokine/chemokine profiles of severe acute respiratory syndrome
Auteurs : YONG JIANG [République populaire de Chine, Hong Kong] ; JUN XU ; CHENGZHI ZHOU ; ZHENGUO WU ; SHUQING ZHONG ; JINGHUA LIU ; WEI LUO ; TAO CHEN ; QINGHE QIN ; PENG DENGSource :
- American journal of respiratory and critical care medicine [ 1073-449X ] ; 2005.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Rationale: There is currently no optimal treatment or effective drug for severe acute respiratory syndrome (SARS), because the immunopathologic mechanism is poorly understood. Objectives: To explore the immune mechanism underlying the pathogenesis of SARS, we studied the expression profile of cytokines/chemokines in the blood and the immunopathology of the lung and lymphoid tissues. Methods: Fourteen cytokines/chemokines in the blood of 23 patients with SARS were dynamically screened, using a bead-based multiassay system. Reverse transcription-polymerase chain reaction was performed to amplify mRNA. Histopathology of the lung and lymphoid tissues at autopsy was examined, using methods of immunohistochemistry and double immunofluorescence staining. Main Results: Interferon-inducible protein-10 (IP-10) was markedly elevated in the blood during the early stage of SARS, and remained at a high level until convalescence. Moreover, IP-10 was highly expressed in both lung and lymphoid tissues, where monocyte-macrophage infiltration and depletion of lymphocytes were observed. The levels of interleukin-6, interleukin-8, and monocyte chemoattractant protein-1 were concomitantly increased in the blood of the patients with superinfection, and the mRNAs for these cytokines were also increased in lung tissues. Conclusions: Induction of IP-10 is a critical event in the initiation of immune-mediated acute lung injury and lymphocyte apoptosis during the development of SARS. Superinfection after the immune injury is the main cause of death. The prompt elevation of interleukin-6, interleukin-8, and monocyte chemoattractant protein-1 is a sign of superinfection, indicating a high risk of death.
Affiliations:
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respiratory syndrome</title><author><name sortKey="Yong Jiang" sort="Yong Jiang" uniqKey="Yong Jiang" last="Yong Jiang">YONG JIANG</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>Key Laboratory of Functional Proteomics of Guangdong Province, Department of Pathophysiology, Southern Medical University, and Guangzhou Institute of Respiratory Diseases</s1><s2>Guangzhou</s2><s3>CHN</s3></inist:fA14><country>République populaire de Chine</country><placeName><settlement type="city">Jiangmen</settlement><region type="province">Guangdong</region></placeName></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Biochemistry, Hong Kong University of Science and Technology</s1><s3>HKG</s3></inist:fA14><country>Hong Kong</country><wicri:noRegion>Department of Biochemistry, Hong Kong University of Science and Technology</wicri:noRegion></affiliation></author><author><name sortKey="Jun Xu" sort="Jun Xu" uniqKey="Jun Xu" last="Jun Xu">JUN XU</name></author><author><name sortKey="Chengzhi Zhou" sort="Chengzhi Zhou" uniqKey="Chengzhi Zhou" last="Chengzhi Zhou">CHENGZHI ZHOU</name></author><author><name sortKey="Zhenguo Wu" sort="Zhenguo Wu" uniqKey="Zhenguo Wu" last="Zhenguo Wu">ZHENGUO WU</name></author><author><name sortKey="Shuqing Zhong" sort="Shuqing Zhong" uniqKey="Shuqing Zhong" last="Shuqing Zhong">SHUQING ZHONG</name></author><author><name sortKey="Jinghua Liu" sort="Jinghua Liu" uniqKey="Jinghua Liu" last="Jinghua Liu">JINGHUA LIU</name></author><author><name sortKey="Wei Luo" sort="Wei Luo" uniqKey="Wei Luo" last="Wei Luo">WEI LUO</name></author><author><name sortKey="Tao Chen" sort="Tao Chen" uniqKey="Tao Chen" last="Tao Chen">TAO CHEN</name></author><author><name sortKey="Qinghe Qin" sort="Qinghe Qin" uniqKey="Qinghe Qin" last="Qinghe Qin">QINGHE QIN</name></author><author><name sortKey="Peng Deng" sort="Peng Deng" uniqKey="Peng Deng" last="Peng Deng">PENG DENG</name></author></analytic><series><title level="j" type="main">American journal of respiratory and critical care medicine</title><title level="j" type="abbreviated">Am. j. respir. crit. care med.</title><idno type="ISSN">1073-449X</idno><imprint><date when="2005">2005</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">American journal of respiratory and critical care medicine</title><title level="j" type="abbreviated">Am. j. respir. crit. care med.</title><idno type="ISSN">1073-449X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Chemokine</term><term>Coronavirus</term><term>Cytokine</term><term>Intensive care</term><term>Resuscitation</term><term>Severe acute respiratory syndrome</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Réanimation</term><term>Soin intensif</term><term>Cytokine</term><term>Chimiokine</term><term>Syndrome respiratoire aigu sévère</term><term>Coronavirus</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Rationale: There is currently no optimal treatment or effective drug for severe acute respiratory syndrome (SARS), because the immunopathologic mechanism is poorly understood. Objectives: To explore the immune mechanism underlying the pathogenesis of SARS, we studied the expression profile of cytokines/chemokines in the blood and the immunopathology of the lung and lymphoid tissues. Methods: Fourteen cytokines/chemokines in the blood of 23 patients with SARS were dynamically screened, using a bead-based multiassay system. Reverse transcription-polymerase chain reaction was performed to amplify mRNA. Histopathology of the lung and lymphoid tissues at autopsy was examined, using methods of immunohistochemistry and double immunofluorescence staining. Main Results: Interferon-inducible protein-10 (IP-10) was markedly elevated in the blood during the early stage of SARS, and remained at a high level until convalescence. Moreover, IP-10 was highly expressed in both lung and lymphoid tissues, where monocyte-macrophage infiltration and depletion of lymphocytes were observed. The levels of interleukin-6, interleukin-8, and monocyte chemoattractant protein-1 were concomitantly increased in the blood of the patients with superinfection, and the mRNAs for these cytokines were also increased in lung tissues. Conclusions: Induction of IP-10 is a critical event in the initiation of immune-mediated acute lung injury and lymphocyte apoptosis during the development of SARS. Superinfection after the immune injury is the main cause of death. The prompt elevation of interleukin-6, interleukin-8, and monocyte chemoattractant protein-1 is a sign of superinfection, indicating a high risk of death.</div></front></TEI><affiliations><list><country><li>Hong Kong</li><li>République populaire de Chine</li></country><region><li>Guangdong</li></region><settlement><li>Jiangmen</li></settlement></list><tree><noCountry><name sortKey="Chengzhi Zhou" sort="Chengzhi Zhou" uniqKey="Chengzhi Zhou" last="Chengzhi Zhou">CHENGZHI ZHOU</name><name sortKey="Jinghua Liu" sort="Jinghua Liu" uniqKey="Jinghua Liu" last="Jinghua Liu">JINGHUA LIU</name><name sortKey="Jun Xu" sort="Jun Xu" uniqKey="Jun Xu" last="Jun Xu">JUN XU</name><name sortKey="Peng Deng" sort="Peng Deng" uniqKey="Peng Deng" last="Peng Deng">PENG DENG</name><name sortKey="Qinghe Qin" sort="Qinghe Qin" uniqKey="Qinghe Qin" last="Qinghe Qin">QINGHE QIN</name><name sortKey="Shuqing Zhong" sort="Shuqing Zhong" uniqKey="Shuqing Zhong" last="Shuqing Zhong">SHUQING ZHONG</name><name sortKey="Tao Chen" sort="Tao Chen" uniqKey="Tao Chen" last="Tao Chen">TAO CHEN</name><name sortKey="Wei Luo" sort="Wei Luo" uniqKey="Wei Luo" last="Wei Luo">WEI LUO</name><name sortKey="Zhenguo Wu" sort="Zhenguo Wu" uniqKey="Zhenguo Wu" last="Zhenguo Wu">ZHENGUO WU</name></noCountry><country name="République populaire de Chine"><region name="Guangdong"><name sortKey="Yong Jiang" sort="Yong Jiang" uniqKey="Yong Jiang" last="Yong Jiang">YONG JIANG</name></region></country><country name="Hong Kong"><noRegion><name sortKey="Yong Jiang" sort="Yong Jiang" uniqKey="Yong Jiang" last="Yong Jiang">YONG JIANG</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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