JCI Insight
. 2020 May 19;138070.
doi: 10.1172/jci.insight.138070. Online ahead of print.
Clinical and Pathological Investigation of Severe COVID-19 Patients
Shaohua Li 1 , Lina Jiang 1 , Xi Li 1 , Fang Lin 2 , Yijin Wang 1 , Boan Li 3 , Tianjun Jiang 4 , Weimin An 5 , Shuhong Liu 1 , Hongyang Liu 1 , Pengfei Xu 1 , Lihua Zhao 1 , Lixin Zhang 1 , Jinsong Mu 2 , Hongwei Wang 6 , Jiarui Kang 6 , Yan Li 1 , Lei Huang 4 , Caizhong Zhu 4 , Shousong Zhao 7 , Jiangyang Lu 6 , Junsheng Ji 4 , Jingmin Zhao 1
Affiliations
- PMID: 32427582
- DOI: 10.1172/jci.insight.138070
Abstract
Background: Severe acute respiratory coronavirus 2 (SARS-CoV-2) caused coronavirus disease 2019 (COVID-19) has become a pandemic. This study addressed the clinical and immunopathological characteristics of severe COVID-19.
Methods: Sixty-nine COVID-19 patients were classified into as severe and non-severe groups to analyze their clinical and laboratory characteristics. A panel of blood cytokines was quantified over time. Biopsy specimens from two deceased cases were obtained for immunopathological, ultrastructural, and in situ hybridization examinations.
Results: Circulating cytokines, including IL8, IL6, TNFα, IP10, MCP1, and RANTES, were significantly elevated in severe COVID-19 patients. Dynamic IL6 and IL8 were associated with disease progression. SARS-CoV-2 was demonstrated to infect type II, type I pneumocytes and endothelial cells, leading to severe lung damage through cell pyroptosis and apoptosis. In severe cases, lymphopenia, neutrophilia, depletion of CD4+ and CD8+ T lymphocytes, and massive macrophage and neutrophil infiltrates were observed in both blood and lung tissues.
Conclusions: A panel of circulating cytokines could be used to predict disease deterioration and inform clinical interventions. Severe pulmonary damage was predominantly attributed to both SARS-CoV-2 caused cytopathy and immunopathologic damage. Strategies that encourage pulmonary recruitment and overactivation of inflammatory cells by suppressing cytokine storm might improve the outcomes of severe COVID-19 patients.
Keywords: Apoptosis; Infectious disease; Macrophages; Medical statistics; Pulmonology.