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Dear Editor, Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV-2) with the symptoms including fever, dry cough and shortness of breath.[1, 2] Most COVID-19 patients will develop mild to moderate symptoms, while some infected people may face to hyper-inflammation induced by massive cytokines/chemokines production, called as cytokine storm, which may lead to fatal pneumonia and acute respiratory distress syndrome.[1, 2] Although, there is no specific antiviral therapy for COVID-19, understanding of cytokine storm mechanism in this disease can help to speculate possible therapeutic interventions.[3] Current reports have presented different cytokine profiles in patients with severe COVID-19.[1, 4–9] For example, the higher levels of interleukin (IL)-2, IL-7, IL-10, tumor necrosis factor (TNF), granulocyte-colony stimulating factor (G-CSF), interferon gamma-induced protein 10 (IP-10; CXCL10), MCP-1 (CCL2) and MIP-1A (CCL3), but not IL-6, have been first shown in intensive care unit (ICU) patients compared to non-ICU patients.[1] Subsequent studies revealed the contribution of other cytokines, including IL-1β, IL-1ra, IL-2R, IL-6, IL-8 (CXCL8), IL-17, interferon (IFN)-γ and GM-CSF (granulocytemacrophage colony-stimulating factor), during severe COVID-19 infections.[4, 5, 8, 9] Figure 1 displays the protein-protein interaction between these cytokines/chemokines. In most existing reports, the elevated levels of several cytokines/chemokine (ie., IL-6, IL-10, IFN-γ, TNF and IP-10), have been greater emphasized in severely ill (ICU) COVID-19 patients than mild to …