2004 | C. K. WONG*, C. W. K. LAM*, A. K. L. WU‡, W. K. IP‡, N. L. S. LEE‡, I. H. S. CHAN‡, L. C. W. LIT‡, D. S. C. HUI‡, M. H. M. CHAN‡, S. S. C. CHUNG§ & J. J. Y. SUNG‡
Severe acute respiratory syndrome (SARS) is a newly emerged infectious disease caused by a novel coronavirus. The study investigated changes in plasma T helper (Th) cell cytokines, inflammatory cytokines, and chemokines in 20 SARS patients. The results showed significant elevation of Th1 cytokine IFN-γ, inflammatory cytokines IL-1, IL-6, and IL-12 for at least 2 weeks after disease onset, but no significant elevation of TNF-α, IL-10, IL-2, or IL-4. Chemokine profiles showed significant elevation of IL-8, MCP-1, and IP-10. Corticosteroid treatment significantly reduced IL-8, MCP-1, and IP-10 concentrations from 5 to 8 days after treatment. These findings confirm the activation of Th1 cell-mediated immunity and hyperinnate inflammatory response in SARS through the accumulation of monocytes/macrophages and neutrophils. The study also found that corticosteroid treatment reduced the levels of these cytokines and chemokines, leading to improvement in clinical condition, pulmonary function, and radiological appearance in SARS patients. The elevation of Th1-related cytokines and inflammatory cytokines, along with chemokines, was associated with disease severity. The study suggests that the elevation of these cytokines and chemokines plays an important role in the immunopathological mechanisms of SARS. The study also highlights the potential of using these cytokines and chemokines as prognostic indicators for disease severity in SARS. The study also suggests that anticytokine/chemokine immunotherapy may represent a novel approach for the treatment of hyperactive inflammation in SARS.Severe acute respiratory syndrome (SARS) is a newly emerged infectious disease caused by a novel coronavirus. The study investigated changes in plasma T helper (Th) cell cytokines, inflammatory cytokines, and chemokines in 20 SARS patients. The results showed significant elevation of Th1 cytokine IFN-γ, inflammatory cytokines IL-1, IL-6, and IL-12 for at least 2 weeks after disease onset, but no significant elevation of TNF-α, IL-10, IL-2, or IL-4. Chemokine profiles showed significant elevation of IL-8, MCP-1, and IP-10. Corticosteroid treatment significantly reduced IL-8, MCP-1, and IP-10 concentrations from 5 to 8 days after treatment. These findings confirm the activation of Th1 cell-mediated immunity and hyperinnate inflammatory response in SARS through the accumulation of monocytes/macrophages and neutrophils. The study also found that corticosteroid treatment reduced the levels of these cytokines and chemokines, leading to improvement in clinical condition, pulmonary function, and radiological appearance in SARS patients. The elevation of Th1-related cytokines and inflammatory cytokines, along with chemokines, was associated with disease severity. The study suggests that the elevation of these cytokines and chemokines plays an important role in the immunopathological mechanisms of SARS. The study also highlights the potential of using these cytokines and chemokines as prognostic indicators for disease severity in SARS. The study also suggests that anticytokine/chemokine immunotherapy may represent a novel approach for the treatment of hyperactive inflammation in SARS.