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lüll Interactions of glucocorticoids and beta 2-agonists Adcock IM; Stevens DA; Barnes PJEur Respir J 1996[Jan]; 9 (1): 160-8Beta 2-adrenoreceptor agonists and glucocorticosteroids are the two most effective treatments for asthma and are often used in combination. Glucocorticoids mediate their anti-inflammatory effects through the action of activated glucocorticoid receptors (GRs). Many of the effects of GRs on the synthesis of cytokines and other inflammatory mediators are due to a direct interaction with other deoxyribonucleic acid (DNA)-binding proteins belonging to the basic leucine zipper (bZIP) group of transcription factors, such as activator protein-1 (AP-1) and nuclear factor-kappa B (NF-kappa B). Beta 2-agonists are potent bronchodilators at low doses and at high doses can activate gene transcription via a bZIP protein, cyclic adenosine monophosphate (cAMP) response element binding protein (CREB). Activated GRs and CREB can interact with each other within the nucleus to modulate both DNA-binding and gene transcription in either a positive or inhibitory manner, depending on cell type. In lung cells, high doses of beta 2-agonists reduce the ability of GR to bind DNA, a process which is mediated by CREB activation. Inhibition of GR DNA-binding by CREB raises the possibility that high-dose beta 2-agonists could have functional antiglucocorticoid activity and may be a basis for the reported increase in asthma morbidity and mortality in industrialized countries, which have increasing per capita beta 2-agonist use.|*Adrenergic beta-2 Receptor Agonists[MESH]|Adrenergic beta-Agonists/*pharmacology/therapeutic use[MESH]|Asthma/drug therapy[MESH]|Cyclic AMP/metabolism[MESH]|Drug Interactions[MESH]|Drug Therapy, Combination[MESH]|Glucocorticoids/adverse effects/*pharmacology/therapeutic use[MESH]|Humans[MESH]|Lung/*drug effects/*metabolism[MESH]|Receptors, Adrenergic, beta-2/genetics[MESH]|Transcription Factors/metabolism[MESH]|Transcription, Genetic/*drug effects[MESH] |