Mechanisms of Action of Glucocorticoids in Bronchial Asthma

Asthma isa major health problem and their incidence is increasingand represent a recognized cause of morbidity and mortality. Glucocorticoids are the most effective drugs for asthma. Glucocorticoids suppress inflammation by several mechanisms. Its principal action at therapeutic doses is due to trans-repression of activated inflammatory genes, by the recruitment of the enzyme histone desacetylase-2 and the subsequent remodeling of chromatin. At higher concentration, glucocorticoids act as trans-activators, acetylating histones and stimulating the transcription of anti-inflammatory genes. Eventually, this mechanism could be involved in the activation of genes related to side effects. Post-transcriptional effects that modulate the stability of mRNA have been proved. This mechanism of action is known as genomic. In the last decades, a mechanism of local action with the use of glucocorticoids involving an interaction between glucocorticoids and noradrenaline has been described, through a membrane receptor in the smooth muscle of the blood vessels that reduces hyperperfusion and mucosal edema. This mechanism is known as non-genomic. This chapter discusses and compares both mechanisms by establishing similarities and differences between the two. Alcibey Alvarado1* and Isabel Arce2 1Department of Internal Medicine and Neumology, Medical Diagnostic Clinic, Costa Rica 2Department of Medicine and General Surgery, University of Costa Rica, Costa Rica *Corresponding author: Alcibey Alvarado, Clínica de Diagnóstico Médico, Torre Médica, San José, Costa Rica, Central América. Tel: 50622237134, 50622566439, 50688783325, 50687351858; Fax: 50622216754; Email: [email protected] Published Date: December 26, 2016