Dysregulated immune response in COVID-19.
Corticosteroid therapy aims to support the central regulatory function of the activated glucocorticoid receptor α (GC-GRα) throughout disease development and resolution. The dysregulated immune response observed in COVID-19 is qualitatively similar to that of multifactorial ARDS [
9]. In patients with severe COVID-19, glucocorticoid receptor expression in bronchoalveolar lavage myeloid cells is negatively related to lung neutrophilic inflammation, NETosis, and severity of symptoms [
10]. Translational research in ARDS patients randomized to methylprednisolone has demonstrated the ability of corticosteroid therapy to rescue the cellular concentrations and functions of activated GC-GRα leading to downregulation of systemic and pulmonary nuclear factor- κB-activated markers of inflammation, coagulation, and fibroproliferation [
11,
12]. Biological improvement was associated with accelerated disease resolution [
11]. Further work is needed to understand the effect of corticosteroid therapy on the immune response to COVID-19.