Inflammatory response and effects of corticosteroids on inflammation. This simplified cartoon illustrates the presumed pathophysiological steps during SARS-COV2 infection. The first step is the infection of type-2 pneumocytes and macrophages with SARS-CoV2 via the ACE-2 receptor, leading to the activation of alveolar macrophages. Activated macrophages release proinflammatory mediators (e.g., IL-1B, IL-6, IL-8 and tumor necrosis factor (TNF)-α) and suppress the anti-inflammatory mediators (e.g., IL-10, IL-1 receptor antagonist (RA)), promoting the infiltration of neutrophils in the alveolus. Toxic mediators are released by these neutrophils and cause further damage to the endothelial–epithelial barrier, initiating additional damage to the endothelial–epithelial barrier. Eventually, damage to these endothelial–epithelial cells, together with the loss of tight junctions and surfactant, leads to the influx of protein-rich fluid edema in the alveolar compartment which impairs gas exchange. Later, fibroblasts start to proliferate and growth factors are produced. This pro-inflammatory response can be suppressed by corticosteroids. Corticosteroids can freely diffuse the plasma membrane to bind to specific receptors. Upon binding to the glucocorticoid receptor (GR), the complex translocates to the nucleus where it interacts with glucocorticoid response elements (GRE), nuclear factor kB (NFKB) and activator protein-1 (AP-1). This interaction results in suppression of pro-inflammatory cytokines synthesis, influx and activation of neutrophils and impairment of macrophage autophagy. As a consequence, patients are more susceptible for secondary infections [3, 49, 50].