tetano
Editor, Senior Moderator
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[SUP] 1 [/SUP], Lina Jiang[SUP] 1 [/SUP], Xi Li[SUP] 1 [/SUP], Fang Lin[SUP] 2 [/SUP], Yijin Wang[SUP] 1 [/SUP], Boan Li[SUP] 3 [/SUP], Tianjun Jiang[SUP] 4 [/SUP], Weimin An[SUP] 5 [/SUP], Shuhong Liu[SUP] 1 [/SUP], Hongyang Liu[SUP] 1 [/SUP], Pengfei Xu[SUP] 1 [/SUP], Lihua Zhao[SUP] 1 [/SUP], Lixin Zhang[SUP] 1 [/SUP], Jinsong Mu[SUP] 2 [/SUP], Hongwei Wang[SUP] 6 [/SUP], Jiarui Kang[SUP] 6 [/SUP], Yan Li[SUP] 1 [/SUP], Lei Huang[SUP] 4 [/SUP], Caizhong Zhu[SUP] 4 [/SUP], Shousong Zhao[SUP] 7 [/SUP], Jiangyang Lu[SUP] 6 [/SUP], Junsheng Ji[SUP] 4 [/SUP], Jingmin Zhao[SUP] 1 [/SUP]
Affiliations
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.
. 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[SUP] 1 [/SUP], Lina Jiang[SUP] 1 [/SUP], Xi Li[SUP] 1 [/SUP], Fang Lin[SUP] 2 [/SUP], Yijin Wang[SUP] 1 [/SUP], Boan Li[SUP] 3 [/SUP], Tianjun Jiang[SUP] 4 [/SUP], Weimin An[SUP] 5 [/SUP], Shuhong Liu[SUP] 1 [/SUP], Hongyang Liu[SUP] 1 [/SUP], Pengfei Xu[SUP] 1 [/SUP], Lihua Zhao[SUP] 1 [/SUP], Lixin Zhang[SUP] 1 [/SUP], Jinsong Mu[SUP] 2 [/SUP], Hongwei Wang[SUP] 6 [/SUP], Jiarui Kang[SUP] 6 [/SUP], Yan Li[SUP] 1 [/SUP], Lei Huang[SUP] 4 [/SUP], Caizhong Zhu[SUP] 4 [/SUP], Shousong Zhao[SUP] 7 [/SUP], Jiangyang Lu[SUP] 6 [/SUP], Junsheng Ji[SUP] 4 [/SUP], Jingmin Zhao[SUP] 1 [/SUP]
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.