The role of the TGF-SMAD signalling pathway in the etiopathogenesis of severe asthma

Abstract

Asthma is a chronic inflammatory heterogeneous disease of the lower respiratory tract characterised by the occurrence of bronchial hyper-responsiveness and paroxysmal, changeable bronchial obstruction. Transforming growth factor-βeta (TGF-β) is one of the cytokines involved in mediating airway inflammation and remodelling. The level of TGF-β1 gene expression correlates with severity of symptoms. Alterations in the main SMAD signal transmission, overexpression of TGF-β genes and changes in the transcriptome cause excessive secretion of TGF-β and its increased expression in target cells, which clinically induces a moderate-severe or severe course of asthma as well as an earlier and faster disease progression. Knowledge of these processes allows clinicians to assess immune responses in patients, which affects adequate disease control and prevention of remodelling.