한빛사 논문
Dong-Min Kim1,15, Yuri Kim2,3,4,15, Jun-Won Seo1,15, Jooyeon Lee5,15, Uni Park2,3,15, Na-Young Ha2,3,4,15, Jaemoon Koh6,15, Hyoree Park2,3, Jae-Won Lee2,3, Hyo-Jin Ro2,3, Na Ra Yun1, Da Young Kim1, Sung Ho Yoon1, Yong Sub Na1, Do Sik Moon1, Sung-Chul Lim7, Choon-Mee Kim8, Kyeongseok Jeon2,3, Jun-Gu Kang9, Na-Yoon Jang2,3, Hyeongseok Jeong5, Jungok Kim10, Shinhyea Cheon5, Kyung Mok Sohn5, Jae Youg Moon10, Sungmin Kym10, Seung Ro Han11, Myung-Shin Lee11, Hyun-Je Kim12, Woong-Yang Park12,13, Ji-Yeob Choi3, Hyun-Woo Shin3, Hye-Young Kim3, Chung-Hyun Cho3, Yoon Kyung Jeon6, Yeon-Sook Kim5,*, Nam-Hyuk Cho2,3,4,14,*
1Department of Internal Medicine, Chosun University College of Medicine, Gwangju 61452, Republic of Korea
2Department of Microbiology and Immunology
3Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Republic of Korea
4Institute of Endemic Disease, Seoul National University Medical Research Center, Seoul 03080, Republic of Korea
5Department of Internal Medicine, Chungnam National University School of Medicine, Daejeon 35015, Republic of Korea
6Department of Pathology, Seoul National University College of Medicine, Seoul 03080, Republic of Korea
7Department of Pathology
8Premedical Science, Chosun University College of Medicine, Gwangju 61452, Republic of Korea
9Korea Zoonosis Research Institute, Jeonbuk National University, Iksan 54531, Republic of Korea
10Department of Internal Medicine, Chungnam National University Sejong Hospital, Sejong 30099, Republic of Korea
11Department of Microbiology and Immunology, Eulji University School of Medicine, Daejeon 34824, Republic of Korea
12Department of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences & Technology, Sungkyunkwan University, Seoul 06351, Republic of Korea
13Geninus Inc., Seoul 05836, Republic of Korea
14Seoul National University Bundang Hospital, Seongnam-si, Gyeonggi-do 13620, Republic of Korea
15These authors contributed equally.
*Corresponding author
Abstract
Despite the worldwide effect of the Coronavirus disease 2019 (COVID-19) pandemic, the underlying mechanisms of fatal viral pneumonia remain elusive. Here, we show that critical COVID-19 is associated with enhanced eosinophil-mediated inflammation when compared to non-critical cases. In addition, we confirm increased Th2-biased adaptive immune responses, accompanying overt complement activation, in the critical group. Moreover, enhanced antibody responses and complement activation is associated with disease pathogenesis as evidenced by formation of immune complexes and membrane attack complexes in airways and vasculature of lung biopsies from six fatal cases, as well as by enhanced hallmark gene set signatures of FcγR signaling and complement activation in myeloid cells of respiratory specimens from critical COVID-19 patients. These results suggest that SARS-CoV-2 infection may drive specific innate immune responses, including eosinophil-mediated inflammation, and subsequent pulmonary pathogenesis via enhanced Th2-biased immune responses, which might be crucial drivers of critical disease in COVID-19 patients.
Keywords : COVID-19, SARS-CoV-2, eosinophilic inflammation, pneumonia
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