Temporal changes in cytokine/chemokine profiles and pulmonary involvement in severe acute respiratory syndrome
Identifieur interne : 004161 ( Main/Exploration ); précédent : 004160; suivant : 004162Temporal changes in cytokine/chemokine profiles and pulmonary involvement in severe acute respiratory syndrome
Auteurs : Jung-Yien Chien ; Po-Ren Hsueh ; Wern-Cherng Cheng ; Chong-Jen Yu [Taïwan] ; Pan-Chyr Yang [Taïwan]Source :
- Respirology [ 1323-7799 ] ; 2006-11.
English descriptors
- Teeft :
- Asian society, Assay, Authors journal compilation, Chemokine, Chemokines, Convalescent stage, Current study, Cytokine, Dendritic cells, Different stages, Dynamic changes, Healthy controls, Internal medicine, Lung injury, Lung involvement, Lymphocyte, Lymphocyte count, National taiwan university hospital, Neutrophil, Normal control samples, Progressive stage, Radiographic, Radiographic score, Radiographic scores, Range days, Respiratory syndrome, Respirology, Sars, Sars infection, Sars patients, Serum levels, Syndrome, Temporal changes, Viral, Viral load, Worst stage.
Abstract
Objective and background: Pathological changes in severe acute respiratory syndrome (SARS) suggest that SARS sequelae are associated with dysregulation of cytokine and chemokine production. To improve understanding of the immuno‐pathological processes involved in lung injury associated with SARS, the temporal changes in cytokine/chemokine profiles in the sera of SARS patients were compared with those of patients with community‐acquired pneumonia (CAP), according to the degree of lung involvement. Methods: Serum levels of 11 cytokines and chemokines, in 14 patients with SARS and 24 patients with CAP, were serially checked using a bead‐based multiassay system. Sera from 12 healthy subjects were used as normal controls. Results: The serum levels of interferon‐γ‐inducible protein‐10 (IP‐10), IL‐2 and IL‐6 were significantly elevated during SARS infection. In patients with CAP, but not in those with SARS, the levels of interferon‐γ, IL‐10, IL‐8 and monokine induced by interferon‐γ (MIG) were significantly elevated compared with the levels in healthy controls. Among the chemokines/cytokines, IL‐6 levels correlated most strongly with radiographic scores (r = 0.62). The elevation of IP‐10 and IL‐2 antedated the development of chest involvement and reached peak levels earlier than the radiographic scores. In contrast, the dynamic changes in IL‐6, C‐reactive protein and neutrophils occurred synchronously with the changes in radiographic scores. The mean ratio of IL‐6 to IL‐10 in SARS patients (4.84; range 0.41–21) was significantly higher than that in CAP patients (2.95; range 0.02–10.57) (P = 0.04). Conclusions: The early induction of IP‐10 and IL‐2, as well as the subsequent over‐production of IL‐6 and lack of IL‐10 production, probably contribute to the main immuno‐pathological processes involved in lung injury in SARS. These changes in cytokine/chemokine profile are remarkably different from those observed in CAP patients.
Url:
DOI: 10.1111/j.1440-1843.2006.00942.x
Affiliations:
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Medical College, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation><affiliation></affiliation></author><author><name sortKey="Yang, Pan Hyr" sort="Yang, Pan Hyr" uniqKey="Yang P" first="Pan-Chyr" last="Yang">Pan-Chyr Yang</name><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Internal Medicine, National Taiwan University Hospital and National Taiwan University Medical College, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Respirology</title><title level="j" type="alt">RESPIROLOGY</title><idno type="ISSN">1323-7799</idno><idno type="eISSN">1440-1843</idno><imprint><biblScope unit="vol">11</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="715">715</biblScope><biblScope unit="page" to="722">722</biblScope><biblScope unit="page-count">8</biblScope><publisher>Blackwell Publishing Asia</publisher><pubPlace>Melbourne, Australia</pubPlace><date type="published" when="2006-11">2006-11</date></imprint><idno type="ISSN">1323-7799</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1323-7799</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Asian society</term><term>Assay</term><term>Authors journal compilation</term><term>Chemokine</term><term>Chemokines</term><term>Convalescent stage</term><term>Current study</term><term>Cytokine</term><term>Dendritic cells</term><term>Different stages</term><term>Dynamic changes</term><term>Healthy controls</term><term>Internal medicine</term><term>Lung injury</term><term>Lung involvement</term><term>Lymphocyte</term><term>Lymphocyte count</term><term>National taiwan university hospital</term><term>Neutrophil</term><term>Normal control samples</term><term>Progressive stage</term><term>Radiographic</term><term>Radiographic score</term><term>Radiographic scores</term><term>Range days</term><term>Respiratory syndrome</term><term>Respirology</term><term>Sars</term><term>Sars infection</term><term>Sars patients</term><term>Serum levels</term><term>Syndrome</term><term>Temporal changes</term><term>Viral</term><term>Viral load</term><term>Worst stage</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Objective and background: Pathological changes in severe acute respiratory syndrome (SARS) suggest that SARS sequelae are associated with dysregulation of cytokine and chemokine production. To improve understanding of the immuno‐pathological processes involved in lung injury associated with SARS, the temporal changes in cytokine/chemokine profiles in the sera of SARS patients were compared with those of patients with community‐acquired pneumonia (CAP), according to the degree of lung involvement. Methods: Serum levels of 11 cytokines and chemokines, in 14 patients with SARS and 24 patients with CAP, were serially checked using a bead‐based multiassay system. Sera from 12 healthy subjects were used as normal controls. Results: The serum levels of interferon‐γ‐inducible protein‐10 (IP‐10), IL‐2 and IL‐6 were significantly elevated during SARS infection. In patients with CAP, but not in those with SARS, the levels of interferon‐γ, IL‐10, IL‐8 and monokine induced by interferon‐γ (MIG) were significantly elevated compared with the levels in healthy controls. Among the chemokines/cytokines, IL‐6 levels correlated most strongly with radiographic scores (r = 0.62). The elevation of IP‐10 and IL‐2 antedated the development of chest involvement and reached peak levels earlier than the radiographic scores. In contrast, the dynamic changes in IL‐6, C‐reactive protein and neutrophils occurred synchronously with the changes in radiographic scores. The mean ratio of IL‐6 to IL‐10 in SARS patients (4.84; range 0.41–21) was significantly higher than that in CAP patients (2.95; range 0.02–10.57) (P = 0.04). Conclusions: The early induction of IP‐10 and IL‐2, as well as the subsequent over‐production of IL‐6 and lack of IL‐10 production, probably contribute to the main immuno‐pathological processes involved in lung injury in SARS. These changes in cytokine/chemokine profile are remarkably different from those observed in CAP patients.</div></front></TEI><affiliations><list><country><li>Taïwan</li></country></list><tree><noCountry><name sortKey="Cheng, Wern Herng" sort="Cheng, Wern Herng" uniqKey="Cheng W" first="Wern-Cherng" last="Cheng">Wern-Cherng Cheng</name><name sortKey="Chien, Jung Ien" sort="Chien, Jung Ien" uniqKey="Chien J" first="Jung-Yien" last="Chien">Jung-Yien Chien</name><name sortKey="Hsueh, Po En" sort="Hsueh, Po En" uniqKey="Hsueh P" first="Po-Ren" last="Hsueh">Po-Ren Hsueh</name></noCountry><country name="Taïwan"><noRegion><name sortKey="Yu, Chong En" sort="Yu, Chong En" uniqKey="Yu C" first="Chong-Jen" last="Yu">Chong-Jen Yu</name></noRegion><name sortKey="Yang, Pan Hyr" sort="Yang, Pan Hyr" uniqKey="Yang P" first="Pan-Chyr" last="Yang">Pan-Chyr Yang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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