Abstract
The efficacy of corticosteroids and its use for the treatment of SARS-CoV-2 infections is controversial. In this study, using data sets of SARS-CoV-2 infected lung tissues and nasopharyngeal swabs, as well as in vitro experiments, we show that SARS-CoV-2 infection significantly downregulates DUSP1 expression. This downregulation of DUSP1 could be the mechanism regulating the enhanced activation of MAPK pathway as well as the reported steroid resistance in SARS-CoV-2 infection. Moreover, chloroquine, an off labeled COVID-19 drug is able to induce DUSP1 and attenuate MAPK pathway; and is expected to improve sensitivity to steroid treatment. However, further mechanistic studies are required to confirm this effect.
Keywords: COVID-19; Chloroquine; Corticosteroid; DUSP1; SARS-CoV-2; p38 MAPK pathway.
【저자키워드】 Corticosteroid, COVID-19, SARS-CoV-2, Chloroquine, DUSP1, p38 MAPK pathway., 【초록키워드】 Corticosteroid, Treatment, Efficacy, Corticosteroids, Chloroquine, SARS-COV-2 infection, sensitivity, nasopharyngeal swabs, pathway, expression, SARS-CoV-2 infections, mechanism, MAPK, DUSP1, steroid, data set, data sets, Activation, lung tissue, downregulation, steroid treatment, IMPROVE, significantly, reported, required, induce, expected, in vitro experiments, downregulate, attenuate, 【제목키워드】 Corticosteroid, sensitivity, pathway, expression, activating, attenuate,