Enhanced eosinophil-mediated inflammation associated with antibody and complement-dependent pneumonic insults in critical COVID-19

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 JangHyeongseok 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

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

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 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.

Original languageEnglish
Article number109798
JournalCell Reports
Volume37
Issue number1
DOIs
StatePublished - 5 Oct 2021

Keywords

  • COVID-19
  • SARS-CoV-2
  • complement
  • eosinophil
  • immune complex
  • pneumonia

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