Prolonged disturbances of in vitro cytokine production in patients with severe acute respiratory syndrome (SARS) treated with ribavirin and steroids
Identifieur interne : 001556 ( Pmc/Checkpoint ); précédent : 001555; suivant : 001557Prolonged disturbances of in vitro cytokine production in patients with severe acute respiratory syndrome (SARS) treated with ribavirin and steroids
Auteurs : B. M. Jones ; E. S. K. Ma ; J. S. M. Peiris ; P. C. Wong ; J. C. M. Ho ; B. Lam ; K. N. Lai ; K. W. T. TsangSource :
- Clinical and Experimental Immunology [ 0009-9104 ] ; 2004.
Abstract
Severe acute respiratory syndrome (SARS) is a new disease which has spread rapidly and widely. We wished to know whether evaluation of
Url:
DOI: 10.1111/j.1365-2249.2003.02391.x
PubMed: 15008980
PubMed Central: 1808981
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<series><title level="j">Clinical and Experimental Immunology</title>
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<front><div type="abstract" xml:lang="en"><title>SUMMARY</title>
<p>Severe acute respiratory syndrome (SARS) is a new disease which has spread rapidly and widely. We wished to know whether evaluation of <italic>in vitro</italic>
cytokine production could contribute to improved understanding of disease pathogenesis and to better patient management. Numbers of unstimulated and mitogen‐stimulated cytokine‐secreting peripheral blood mononuclear cells were measured repeatedly during and after hospitalization in 13 patients with SARS using enzyme‐linked immunospot technology. Numbers of interferon‐gamma, interleukin (IL)‐2, IL‐4, IL‐10 and IL‐12 secreting cells induced by T cell activators were below normal in many or most patients before and during treatment with corticosteroids and ribavirin but returned essentially to normal after completion of treatment. <italic>Staphylococcus aureus</italic>
Cowan 1 (SAC)‐stimulated IL‐10 secreting cells were increased in early SARS but fell during treatment. SAC‐induced IL‐12 secreting cells were deficient before, during and long after treatment. Numbers of cells induced to produce IL‐6 and tumour necrosis factor‐alpha by T cell or monocyte activators were higher than normal in many early SARS patients and were still increased in some during and after treatment. We conclude that prolonged dysregulated cytokine production occurs in SARS and that future studies should be directed at improving anti‐inflammatory and antiviral therapies in order to limit cytokine impairment.</p>
</div>
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<front><journal-meta><journal-id journal-id-type="nlm-ta">Clin Exp Immunol</journal-id>
<journal-id journal-id-type="iso-abbrev">Clin. Exp. Immunol</journal-id>
<journal-id journal-id-type="doi">10.1111/(ISSN)1365-2249</journal-id>
<journal-id journal-id-type="publisher-id">CEI</journal-id>
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<issn pub-type="ppub">0009-9104</issn>
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<publisher><publisher-name>Blackwell Science Ltd</publisher-name>
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<article-id pub-id-type="pmc">1808981</article-id>
<article-id pub-id-type="doi">10.1111/j.1365-2249.2003.02391.x</article-id>
<article-id pub-id-type="publisher-id">CEI2391</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Clinical Studies</subject>
</subj-group>
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<title-group><article-title>Prolonged disturbances of <italic>in vitro</italic>
cytokine production in patients with severe acute respiratory syndrome (SARS) treated with ribavirin and steroids</article-title>
<alt-title alt-title-type="left-running-head">B. M. Jones <italic>et al.</italic>
</alt-title>
<alt-title alt-title-type="right-running-head">Cytokines in SARS</alt-title>
</title-group>
<contrib-group><contrib id="cr1" contrib-type="author" corresp="yes"><name><surname>JONES</surname>
<given-names>B. M.</given-names>
</name>
<xref ref-type="aff" rid="a1"><sup>1</sup>
</xref>
</contrib>
<contrib id="cr2" contrib-type="author"><name><surname>MA</surname>
<given-names>E. S. K.</given-names>
</name>
<xref ref-type="aff" rid="a1"><sup>1</sup>
</xref>
</contrib>
<contrib id="cr3" contrib-type="author"><name><surname>PEIRIS</surname>
<given-names>J. S. M.</given-names>
</name>
<xref ref-type="aff" rid="a2"><sup>2</sup>
</xref>
</contrib>
<contrib id="cr4" contrib-type="author"><name><surname>WONG</surname>
<given-names>P. C.</given-names>
</name>
<xref ref-type="aff" rid="a3"><sup>3</sup>
</xref>
</contrib>
<contrib id="cr5" contrib-type="author"><name><surname>HO</surname>
<given-names>J. C. M.</given-names>
</name>
<xref ref-type="aff" rid="a3"><sup>3</sup>
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<contrib id="cr6" contrib-type="author"><name><surname>LAM</surname>
<given-names>B.</given-names>
</name>
<xref ref-type="aff" rid="a3"><sup>3</sup>
</xref>
</contrib>
<contrib id="cr7" contrib-type="author"><name><surname>LAI</surname>
<given-names>K. N.</given-names>
</name>
<xref ref-type="aff" rid="a3"><sup>3</sup>
</xref>
</contrib>
<contrib id="cr8" contrib-type="author"><name><surname>TSANG</surname>
<given-names>K. W. T.</given-names>
</name>
<xref ref-type="aff" rid="a3"><sup>3</sup>
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<aff id="a1"><label><sup>1</sup>
</label>
University Departments of Pathology,</aff>
<aff id="a2"><label><sup>2</sup>
</label>
Microbiology and</aff>
<aff id="a3"><label><sup>3</sup>
</label>
Medicine, The University of Hong Kong, Queen Mary Hospital, China</aff>
<author-notes><corresp id="correspondenceTo"><label>*</label>
Brian M. Jones PhD, Division of Clinical Immunology, Department of Pathology, Queen Mary Hospital, Pokfulam Road, Hong Kong Special Administrative, Region, China.
E‐mail: <email>bmjones@ha.org.hk</email>
</corresp>
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<pub-date pub-type="epub"><day>05</day>
<month>2</month>
<year>2004</year>
</pub-date>
<pub-date pub-type="ppub"><month>3</month>
<year>2004</year>
</pub-date>
<volume>135</volume>
<issue>3</issue>
<issue-id pub-id-type="doi">10.1111/cei.2004.135.issue-3</issue-id>
<fpage>467</fpage>
<lpage>473</lpage>
<history><pmc-comment>supplied string: (Accepted for publication 18 December 2003)</pmc-comment>
<date date-type="accepted"><day>18</day>
<month>12</month>
<year>2003</year>
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<permissions><license><license-p>This article is being made freely available through PubMed Central as part of the COVID-19 public health emergency response. It can be used for unrestricted research re-use and analysis in any form or by any means with acknowledgement of the original source, for the duration of the public health emergency.</license-p>
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<abstract><title>SUMMARY</title>
<p>Severe acute respiratory syndrome (SARS) is a new disease which has spread rapidly and widely. We wished to know whether evaluation of <italic>in vitro</italic>
cytokine production could contribute to improved understanding of disease pathogenesis and to better patient management. Numbers of unstimulated and mitogen‐stimulated cytokine‐secreting peripheral blood mononuclear cells were measured repeatedly during and after hospitalization in 13 patients with SARS using enzyme‐linked immunospot technology. Numbers of interferon‐gamma, interleukin (IL)‐2, IL‐4, IL‐10 and IL‐12 secreting cells induced by T cell activators were below normal in many or most patients before and during treatment with corticosteroids and ribavirin but returned essentially to normal after completion of treatment. <italic>Staphylococcus aureus</italic>
Cowan 1 (SAC)‐stimulated IL‐10 secreting cells were increased in early SARS but fell during treatment. SAC‐induced IL‐12 secreting cells were deficient before, during and long after treatment. Numbers of cells induced to produce IL‐6 and tumour necrosis factor‐alpha by T cell or monocyte activators were higher than normal in many early SARS patients and were still increased in some during and after treatment. We conclude that prolonged dysregulated cytokine production occurs in SARS and that future studies should be directed at improving anti‐inflammatory and antiviral therapies in order to limit cytokine impairment.</p>
</abstract>
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<tree><noCountry><name sortKey="Ho, J C M" sort="Ho, J C M" uniqKey="Ho J" first="J. C. M." last="Ho">J. C. M. Ho</name>
<name sortKey="Jones, B M" sort="Jones, B M" uniqKey="Jones B" first="B. M." last="Jones">B. M. Jones</name>
<name sortKey="Lai, K N" sort="Lai, K N" uniqKey="Lai K" first="K. N." last="Lai">K. N. Lai</name>
<name sortKey="Lam, B" sort="Lam, B" uniqKey="Lam B" first="B." last="Lam">B. Lam</name>
<name sortKey="Ma, E S K" sort="Ma, E S K" uniqKey="Ma E" first="E. S. K." last="Ma">E. S. K. Ma</name>
<name sortKey="Peiris, J S M" sort="Peiris, J S M" uniqKey="Peiris J" first="J. S. M." last="Peiris">J. S. M. Peiris</name>
<name sortKey="Tsang, K W T" sort="Tsang, K W T" uniqKey="Tsang K" first="K. W. T." last="Tsang">K. W. T. Tsang</name>
<name sortKey="Wong, P C" sort="Wong, P C" uniqKey="Wong P" first="P. C." last="Wong">P. C. Wong</name>
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