Abstract
Coronavirus Disease 2019 (COVID-19) pneumonia is a life-threatening infectious disease, especially for elderly patients with multiple comorbidities. Despite enormous efforts to understand its underlying etiopathogenic mechanisms, most of them remain elusive. In this study, we compared differential plasma miRNAs and cytokines profiles between COVID-19 and other community-acquired pneumonias (CAP). A first screening and subsequent validation assays in an independent cohort of patients revealed a signature of 15 dysregulated miRNAs between COVID-19 and CAP patients. Additionally, multivariate analysis displayed a combination of 4 miRNAs (miR-106b-5p, miR-221-3p, miR-25-3p and miR-30a-5p) that significantly discriminated between both pathologies. Search for targets of these miRNAs, combined with plasma protein measurements, identified a differential cytokine signature between COVID-19 and CAP that included EGFR, CXCL12 and IL-10. Significant differences were also detected in plasma levels of CXCL12, IL-17, TIMP-2 and IL-21R between mild and severe COVID-19 patients. These findings provide new insights into the etiopathological mechanisms underlying COVID-19.
Highlights
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is responsible for the disease known as coronavirus disease 2019 (COVID-19) [1]
Cohort Selection and Clinical Features of Study Populations miRNA profile was assessed in a discovery cohort that consisted of 38 COVID-19 patients (20 with mild and 18 with severe disease), collected during the first wave of the pandemic in Spain, from March to April 2020
High blood pressure (HBP) and dyslipidemia (DL) were the most common comorbidities found in the COVID-19 cohort (34.2% and 29% respectively)
Summary
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is responsible for the disease known as coronavirus disease 2019 (COVID-19) [1]. Initially COVID-19 was defined as a low tract respiratory disease, it is acknowledged as a complex disorder that compromises multiple organs and may cause longlasting damage even in patients that overcome the acute phase [2]. Major efforts have been devoted to identifying molecules able to predict the severity of COVID-19. These efforts were aimed to improve patient stratification and make a better use of the available resources to optimise health care. Dysregulation of other cytokines, including IL-2, IL-10, Interferon (IFN)-g, monocyte chemoattractant protein (MCP)-1 or C-X-C Motif Chemokine Ligand (CXCL) in COVID-19 patients have been reported [5]
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