Critical Care (Jul 2021)

The predicting roles of carcinoembryonic antigen and its underlying mechanism in the progression of coronavirus disease 2019

  • Runzhi Huang,
  • Tong Meng,
  • Qiongfang Zha,
  • Kebin Cheng,
  • Xin Zhou,
  • Junhua Zheng,
  • Dingyu Zhang,
  • Ruilin Liu

DOI
https://doi.org/10.1186/s13054-021-03661-y
Journal volume & issue
Vol. 25, no. 1
pp. 1 – 20

Abstract

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Abstract Background The coronavirus disease 2019 (COVID-19) has induced a worldwide epidemiological event with a high infectivity and mortality. However, the predicting biomarkers and their potential mechanism in the progression of COVID-19 are not well known. Objective The aim of this study is to identify the candidate predictors of COVID-19 and investigate their underlying mechanism. Methods The retrospective study was conducted to identify the potential laboratory indicators with prognostic values of COVID-19 disease. Then, the prognostic nomogram was constructed to predict the overall survival of COVID-19 patients. Additionally, the scRNA-seq data of BALF and PBMCs from COVID-19 patients were downloaded to investigate the underlying mechanism of the most important prognostic indicators in lungs and peripherals, respectively. Results In total, 304 hospitalized adult COVID-19 patients in Wuhan Jinyintan Hospital were included in the retrospective study. CEA was the only laboratory indicator with significant difference in the univariate (P < 0.001) and multivariate analysis (P = 0.020). The scRNA-seq data of BALF and PBMCs from COVID-19 patients were downloaded to investigate the underlying mechanism of CEA in lungs and peripherals, respectively. The results revealed the potential roles of CEA were significantly distributed in type II pneumocytes of BALF and developing neutrophils of PBMCs, participating in the progression of COVID-19 by regulating the cell–cell communication. Conclusion This study identifies the prognostic roles of CEA in COVID-19 patients and implies the potential roles of CEACAM8-CEACAM6 in the progression of COVID-19 by regulating the cell–cell communication of developing neutrophils and type II pneumocyte.

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