Plasma inflammatory cytokines and chemokines in severe acute respiratory syndrome

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ID: 295282
2004
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Abstract
Severe acute respiratory syndrome (SARS) is a recently emerged infectious disease caused by a novel coronavirus, but its immunopathological mechanisms have not yet been fully elucidated. We investigated changes in plasma T helper (Th) cell cytokines, inflammatory cytokines and chemokines in 20 patients diagnosed with SARS. Cytokine profile of SARS patients showed marked elevation of Th1 cytokine interferon (IFN)-gamma, inflammatory cytokines interleukin (IL)-1, IL-6 and IL-12 for at least 2 weeks after disease onset, but there was no significant elevation of inflammatory cytokine tumour necrosis factor (TNF)-alpha, anti-inflammatory cytokine IL-10, Th1 cytokine IL-2 and Th2 cytokine IL-4. The chemokine profile demonstrated significant elevation of neutrophil chemokine IL-8, monocyte chemoattractant protein-1 (MCP-1), and Th1 chemokine IFN-gamma-inducible protein-10 (IP-10). Corticosteroid reduced significantly IL-8, MCP-1 and IP-10 concentrations from 5 to 8 days after treatment (all P < 0.001). Together, the elevation of Th1 cytokine IFN-gamma, inflammatory cytokines IL-1, IL-6 and IL-12 and chemokines IL-8, MCP-1 and IP-10 confirmed the activation of Th1 cell-mediated immunity and hyperinnate inflammatory response in SARS through the accumulation of monocytes/macrophages and neutrophils.
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Authors Chun Kwok Wong, Charles Lam, Alan Wu, Wai‐Ki Ip, Nelson Lee, I Chan, Lydia C.W. Lit, David S.C. Hui, Michael Chan, Enders K. Ng, Joseph J.�Y. Sung
Journal Clinical & Experimental Immunology
Year 2004
DOI
10.1111/j.1365-2249.2004.02415.x
URL
https://academic.oup.com/cei/article-pdf/136/1/95/42146684/j.1365-2249.2004.02415.x.pdf
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