Asthma is a chronic airway disorder principally characterized by bronchial hyperreactivity and airflow obstruction. Increased epithelial and smooth muscle thickness, goblet cell hyperplasia, increased mucus secretion, abnormal deposition of extracellular matrix (ECM) components in the basement membrane (BM) layer and angiogenesis are all events which occur in asthma and are defined with the general term of remodeling. This is an important feature whose repetition and regeneration may bring to an abnormal or exaggerated response to airway insults. One of the characteristic aspects of asthma is an alteration in structural cell function. Airway smooth muscle cells (ASM), myofibroblasts and fibroblasts have the ability to secrete immunomodulatory cytokines and chemokines and to express cell surface receptors. These elements are all important for cell adhesion and leukocyte activation and may be integral components of the inflammatory response as well. In particular cells such as fibroblasts and myofibroblasts, important regulators in the development and maintenance of allergic airway inflammation, have been studied in depth by our group and several studies regarding their role in asthma therapy have been analyzed.