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Sci Rep ; 12(1):21227, 2022.
Article in English | PubMed | ID: covidwho-2151083


Although nearly a fifth of symptomatic COVID-19 patients suffers from severe pulmonary inflammation, the mechanism of developing severe illness is not yet fully understood. To identify significantly altered genes in severe COVID-19, we generated messenger RNA and micro-RNA profiling data of peripheral blood mononuclear cells (PBMCs) from five COVID-19 patients (2 severe and 3 mild patients) and three healthy controls (HC). For further evaluation, two publicly available RNA-Seq datasets (GSE157103 and GSE152418) and one single-cell RNA-Seq dataset (GSE174072) were employed. Based on RNA-Seq datasets, thrombospondin 1 (THBS1) and interleukin-17 receptor A (IL17RA) were significantly upregulated in severe COVID-19 patients' blood. From single-cell RNA-sequencing data, IL17RA level is increased in monocytes and neutrophils, whereas THBS1 level is mainly increased in the platelets. Moreover, we identified three differentially expressed microRNAs in severe COVID-19 using micro-RNA sequencings. Intriguingly, hsa-miR-29a-3p significantly downregulated in severe COVID-19 was predicted to bind the 3'-untranslated regions of both IL17RA and THBS1 mRNAs. Further validation analysis of our cohort (8 HC, 7 severe and 8 mild patients) showed that THBS1, but not IL17RA, was significantly upregulated, whereas hsa-miR-29a-3p was downregulated, in PBMCs from severe patients. These findings strongly suggest that dysregulated expression of THBS1, IL17RA, and hsa-miR-29a-3p involves severe COVID-19.

Journal of Bacteriology and Virology ; 51(3):89-102, 2021.
Article in English | Scopus | ID: covidwho-1538679


The ongoing coronavirus disease-2019 (COVID-19) pandemic is caused by severe acute respiratory syndrome coronavirus-2. COVID-19 severity is related to the cytokine storm phenomenon, which is amplified by pro-inflammatory cytokines and chemokines;it may cause extensive pulmonary damage. Among these cytokines, interleukin (IL)-17, produced mainly by T helper 17 (Th17) cells, is responsible for the immunopathological responses present in acute respiratory distress syndrome. This review discusses the roles of IL-17 and Th17 responses in the pathophysiology of COVID-19. Dysregulated Th17-responses, linked to various risk factors, may contribute to pathological inflammation through the amplification of multiple inflammatory cytokines and chemokines, as well as augmentation of neutrophil infiltration in the lungs of severe COVID-19 patients. A more detailed understanding of the roles of Th17 responses, as well as the mechanisms underlying altered IL-17 production and signaling, may improve therapeutic strategies for severe or critically ill COVID-19 patients by targeting the IL-17 pathway. © 2021 Journal of Bacteriology and Virology.