[Alternations of bronchial smooth muscle and effect of therapy on remodeling in asthma]

Abstract

Alternations in airway wall architecture, particularly increased smooth muscle mass are associated with pathogenesis of asthma. Muscle fiber hyperplasia and hypertrophy is a major contributor to the increase in smooth muscle mass. Airway smooth muscle was traditionally considered to have only contractile and proliferative functions and has little attention with regard to its ability to express and release inflammatory mediators. Airway smooth muscle cells have been shown to release cytokines such as: GM-CSF, IL-11, IL-6, IL-1, IL-5, IL-8, PGs and NO. Airway remodeling has been shown to respond to some degree anti-inflammatory therapy. Several study results indicate that steroid can positively influence progressive airflow limitation. Combined use of a beta2-agonist and steroid can reduced the remodeling progression.