Fatal outcome of severe fever with thrombocytopenia syndrome (SFTS) and severe and critical COVID‐19 is associated with the hyperproduction of IL‐10 and IL‐6 and the low production of TGF‐β
Su Yeon Kang, Jeong Rae Yoo, Yejin Park, So‐Hee Kim, Sang Taek Heo, Seong Hyeon Park, Mi-Sun Kim, Tae‐Jin Kim, Songhyeok Oh, Moo‐Seung Lee, Jung Mogg Kim, Nam‐Hyuk Cho, Kyung‐Mi Lee, Keun‐Hwa Lee, Keun Hwa Lee, Keun Hwa Lee
Abstract
Severe fever with thrombocytopenia syndrome virus (SFTSV) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can cause the hyperproduction of inflammatory cytokines, which have pathological effects in patient including severe or fatal cytokine storms. To characterize the effect of SFTSV and SARS-CoV-2 infection on the production of cytokines in severe fever with thrombocytopenia syndrome (SFTS) and COVID-19 patients, we performed an analysis of cytokines in SFTS and COVID-19 patients and also investigated the role of interleukin-10 (IL-10) in vitro studies: lipopolysaccharide-induced THP-1-derived macrophages, SFTSV infection of THP-1 cells, and SARS-CoV-2 infection of THP-1 cells. In this study, we found that levels of both IL-10 and IL-6 were significantly elevated, the level of transforming growth factor-β (TGF-β) was significantly decreased and IL-10 was elevated earlier than IL-6 in severe and critical COVID-19 and fatal SFTS patients, and inhibition of IL-10 signaling decreased the production of IL-6 and elevated that of TGF-β. Therefore, the hyperproduction of IL-10 and IL-6 and the low production of TGF-β have been linked to cytokine storm-induced mortality in fatal SFTS and severe and critically ill COVID-19 patients and that IL-10 can play an important role in the host immune response to severe and critical SARS-CoV-2 and fatal SFTSV infection.