Enhanced eosinophil-mediated inflammation associated with antibody and complement-dependent pneumonic insults in critical COVID-19
Summary: 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 addi...
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| Format: | Article |
| Language: | English |
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Elsevier
2021-10-01
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| Series: | Cell Reports |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2211124721012584 |
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doaj-87e3e23419fc4f3d9731ab491ab31be6 |
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| record_format |
Article |
| collection |
DOAJ |
| language |
English |
| format |
Article |
| sources |
DOAJ |
| author |
Dong-Min Kim Yuri Kim Jun-Won Seo Jooyeon Lee Uni Park Na-Young Ha Jaemoon Koh Hyoree Park Jae-Won Lee Hyo-Jin Ro Na Ra Yun Da Young Kim Sung Ho Yoon Yong Sub Na Do Sik Moon Sung-Chul Lim Choon-Mee Kim Kyeongseok Jeon Jun-Gu Kang Na-Yoon Jang Hyeongseok Jeong Jungok Kim Shinhyea Cheon Kyung Mok Sohn Jae Youg Moon Sungmin Kym Seung Ro Han Myung-Shin Lee Hyun-Je Kim Woong-Yang Park Ji-Yeob Choi Hyun-Woo Shin Hye-Young Kim Chung-Hyun Cho Yoon Kyung Jeon Yeon-Sook Kim Nam-Hyuk Cho |
| spellingShingle |
Dong-Min Kim Yuri Kim Jun-Won Seo Jooyeon Lee Uni Park Na-Young Ha Jaemoon Koh Hyoree Park Jae-Won Lee Hyo-Jin Ro Na Ra Yun Da Young Kim Sung Ho Yoon Yong Sub Na Do Sik Moon Sung-Chul Lim Choon-Mee Kim Kyeongseok Jeon Jun-Gu Kang Na-Yoon Jang Hyeongseok Jeong Jungok Kim Shinhyea Cheon Kyung Mok Sohn Jae Youg Moon Sungmin Kym Seung Ro Han Myung-Shin Lee Hyun-Je Kim Woong-Yang Park Ji-Yeob Choi Hyun-Woo Shin Hye-Young Kim Chung-Hyun Cho Yoon Kyung Jeon Yeon-Sook Kim Nam-Hyuk Cho Enhanced eosinophil-mediated inflammation associated with antibody and complement-dependent pneumonic insults in critical COVID-19 Cell Reports COVID-19 SARS-CoV-2 eosinophil pneumonia immune complex complement |
| author_facet |
Dong-Min Kim Yuri Kim Jun-Won Seo Jooyeon Lee Uni Park Na-Young Ha Jaemoon Koh Hyoree Park Jae-Won Lee Hyo-Jin Ro Na Ra Yun Da Young Kim Sung Ho Yoon Yong Sub Na Do Sik Moon Sung-Chul Lim Choon-Mee Kim Kyeongseok Jeon Jun-Gu Kang Na-Yoon Jang Hyeongseok Jeong Jungok Kim Shinhyea Cheon Kyung Mok Sohn Jae Youg Moon Sungmin Kym Seung Ro Han Myung-Shin Lee Hyun-Je Kim Woong-Yang Park Ji-Yeob Choi Hyun-Woo Shin Hye-Young Kim Chung-Hyun Cho Yoon Kyung Jeon Yeon-Sook Kim Nam-Hyuk Cho |
| author_sort |
Dong-Min Kim |
| title |
Enhanced eosinophil-mediated inflammation associated with antibody and complement-dependent pneumonic insults in critical COVID-19 |
| title_short |
Enhanced eosinophil-mediated inflammation associated with antibody and complement-dependent pneumonic insults in critical COVID-19 |
| title_full |
Enhanced eosinophil-mediated inflammation associated with antibody and complement-dependent pneumonic insults in critical COVID-19 |
| title_fullStr |
Enhanced eosinophil-mediated inflammation associated with antibody and complement-dependent pneumonic insults in critical COVID-19 |
| title_full_unstemmed |
Enhanced eosinophil-mediated inflammation associated with antibody and complement-dependent pneumonic insults in critical COVID-19 |
| title_sort |
enhanced eosinophil-mediated inflammation associated with antibody and complement-dependent pneumonic insults in critical covid-19 |
| publisher |
Elsevier |
| series |
Cell Reports |
| issn |
2211-1247 |
| publishDate |
2021-10-01 |
| description |
Summary: 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 T helper (Th)2-biased adaptive immune responses, accompanying overt complement activation, in the critical group. Moreover, enhanced antibody responses and complement activation are 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 Fcγ receptor (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. |
| topic |
COVID-19 SARS-CoV-2 eosinophil pneumonia immune complex complement |
| url |
http://www.sciencedirect.com/science/article/pii/S2211124721012584 |
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| _version_ |
1716839990174941184 |
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doaj-87e3e23419fc4f3d9731ab491ab31be62021-10-07T04:24:58ZengElsevierCell Reports2211-12472021-10-01371109798Enhanced eosinophil-mediated inflammation associated with antibody and complement-dependent pneumonic insults in critical COVID-19Dong-Min Kim0Yuri Kim1Jun-Won Seo2Jooyeon Lee3Uni Park4Na-Young Ha5Jaemoon Koh6Hyoree Park7Jae-Won Lee8Hyo-Jin Ro9Na Ra Yun10Da Young Kim11Sung Ho Yoon12Yong Sub Na13Do Sik Moon14Sung-Chul Lim15Choon-Mee Kim16Kyeongseok Jeon17Jun-Gu Kang18Na-Yoon Jang19Hyeongseok Jeong20Jungok Kim21Shinhyea Cheon22Kyung Mok Sohn23Jae Youg Moon24Sungmin Kym25Seung Ro Han26Myung-Shin Lee27Hyun-Je Kim28Woong-Yang Park29Ji-Yeob Choi30Hyun-Woo Shin31Hye-Young Kim32Chung-Hyun Cho33Yoon Kyung Jeon34Yeon-Sook Kim35Nam-Hyuk Cho36Department of Internal Medicine, Chosun University College of Medicine, Gwangju 61452, Republic of KoreaDepartment of Microbiology and Immunology, Seoul National University College of Medicine, Seoul 03080, Republic of Korea; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Republic of Korea; Institute of Endemic Disease, Seoul National University Medical Research Center, Seoul 03080, Republic of KoreaDepartment of Internal Medicine, Chosun University College of Medicine, Gwangju 61452, Republic of KoreaDepartment of Internal Medicine, Chungnam National University School of Medicine, Daejeon 35015, Republic of KoreaDepartment of Microbiology and Immunology, Seoul National University College of Medicine, Seoul 03080, Republic of Korea; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Republic of KoreaDepartment of Microbiology and Immunology, Seoul National University College of Medicine, Seoul 03080, Republic of Korea; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Republic of Korea; Institute of Endemic Disease, Seoul National University Medical Research Center, Seoul 03080, Republic of KoreaDepartment of Pathology, Seoul National University College of Medicine, Seoul 03080, Republic of KoreaDepartment of Microbiology and Immunology, Seoul National University College of Medicine, Seoul 03080, Republic of Korea; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Republic of KoreaDepartment of Microbiology and Immunology, Seoul National University College of Medicine, Seoul 03080, Republic of Korea; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Republic of KoreaDepartment of Microbiology and Immunology, Seoul National University College of Medicine, Seoul 03080, Republic of Korea; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Republic of KoreaDepartment of Internal Medicine, Chosun University College of Medicine, Gwangju 61452, Republic of KoreaDepartment of Internal Medicine, Chosun University College of Medicine, Gwangju 61452, Republic of KoreaDepartment of Internal Medicine, Chosun University College of Medicine, Gwangju 61452, Republic of KoreaDepartment of Internal Medicine, Chosun University College of Medicine, Gwangju 61452, Republic of KoreaDepartment of Internal Medicine, Chosun University College of Medicine, Gwangju 61452, Republic of KoreaDepartment of Pathology, Chosun University College of Medicine, Gwangju 61452, Republic of KoreaPremedical Science, Chosun University College of Medicine, Gwangju 61452, Republic of KoreaDepartment of Microbiology and Immunology, Seoul National University College of Medicine, Seoul 03080, Republic of Korea; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Republic of KoreaKorea Zoonosis Research Institute, Jeonbuk National University, Iksan 54531, Republic of KoreaDepartment of Microbiology and Immunology, Seoul National University College of Medicine, Seoul 03080, Republic of Korea; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Republic of KoreaDepartment of Internal Medicine, Chungnam National University School of Medicine, Daejeon 35015, Republic of KoreaDepartment of Internal Medicine, Chungnam National University Sejong Hospital, Sejong 30099, Republic of KoreaDepartment of Internal Medicine, Chungnam National University School of Medicine, Daejeon 35015, Republic of KoreaDepartment of Internal Medicine, Chungnam National University School of Medicine, Daejeon 35015, Republic of KoreaDepartment of Internal Medicine, Chungnam National University Sejong Hospital, Sejong 30099, Republic of KoreaDepartment of Internal Medicine, Chungnam National University Sejong Hospital, Sejong 30099, Republic of KoreaDepartment of Microbiology and Immunology, Eulji University School of Medicine, Daejeon 34824, Republic of KoreaDepartment of Microbiology and Immunology, Eulji University School of Medicine, Daejeon 34824, Republic of KoreaDepartment of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences & Technology, Sungkyunkwan University, Seoul 06351, Republic of KoreaDepartment of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences & Technology, Sungkyunkwan University, Seoul 06351, Republic of Korea; Geninus Inc., Seoul 05836, Republic of KoreaDepartment of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Republic of KoreaDepartment of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Republic of KoreaDepartment of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Republic of KoreaDepartment of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Republic of KoreaDepartment of Pathology, Seoul National University College of Medicine, Seoul 03080, Republic of KoreaDepartment of Internal Medicine, Chungnam National University School of Medicine, Daejeon 35015, Republic of Korea; Corresponding authorDepartment of Microbiology and Immunology, Seoul National University College of Medicine, Seoul 03080, Republic of Korea; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Republic of Korea; Institute of Endemic Disease, Seoul National University Medical Research Center, Seoul 03080, Republic of Korea; Seoul National University Bundang Hospital, Seongnam-si, Gyeonggi-do 13620, Republic of Korea; Corresponding authorSummary: 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 T helper (Th)2-biased adaptive immune responses, accompanying overt complement activation, in the critical group. Moreover, enhanced antibody responses and complement activation are 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 Fcγ receptor (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.http://www.sciencedirect.com/science/article/pii/S2211124721012584COVID-19SARS-CoV-2eosinophilpneumoniaimmune complexcomplement |