The possible mechanism for this was that the anti-inflammatory effects mediated by glucocorticoid receptors could stabilize the lysosomal membrane, reduce pulmonary vascular permeability, reduce pulmonary leukocyte exudate and alveolar membrane edema, improve the alveolar ventilation/perfusion ratio, control macrophage phagocytosis of the antigen, improve SIRS, reduce pulmonary vascular resistance, and correct shock. This evidence concerns the gene NR3C1 and systemic inflammatory response syndrome.