1. The classic anti-inflammatory or genomic action implicates the activation or repression of multiple genes involved in the inflammatory process. Thus, CS produce their effects on cells by activating glucocorticoid receptors that alter transcription through direct DNA binding. In addition, ligand activated glucocorticoid receptor (GR) can bind pro-inflammatory transcription factors like NFkB (Nuclear Factor kappa B) or activating protein-1 leading to their inactivation. Consequently, CS increase the synthesis of anti-inflammatory proteins, or inhibit the synthesis of many inflammatory proteins through activation or suppression of the genes that encode them. Moreover, CS has been shown to block the production of several pro-inflammatory cytokines by increasing their mRNA (messenger ribonucleic acid) degradation rate. These effects occur with a time lag of about 4-24 hours. So far all the recommended uses of CS in asthma therapy are related to this mode of action, including the use of systemic CS in patients with asthma exacerbation in the emergency room.