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-beta (TGF-b) is one of the cytokines involved in mediating airway inflammation and remodelling. The level of TGF-b1 gene expression correlates with severity of symptoms. Alterations in the main SMAD signal transmission, overexpression of TGF-b genes and changes in the transcriptome cause excessive secretion of TGF-b 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.
Highlights
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
Nowadays five types of isoforms of this factor have been identified, there are only three isoforms found in the human body (TGF-b1, TGF-b2, TGF-b3), each one coded by separate genes
ActR — activin receptor; ALK — anaplastic lymphoma kinase; AP-1 — activator protein 1; ATF-2 — activating transcription factor 2; bone morphogenetic proteins (BMPs) — bone morphogenetic protein; BMPR — bone morphogenetic protein receptor; CBFA — core-binding factor A; CREB — cyclic AMP-regulated enhancer-binding protein; FAST — forkhead activin signal transducer; IgA — immunoglobulin type A; growth differentiation factors (GDFs) — growth differentation factor; LEF1 — lymphoid enhancer-binding factor 1; Nodal-lefty — nodal left-right determination factors; PAI-1 — plasminogen activator inhibitor-1; Staphylococcus aureus Cowan 1 (SAC) — Staphylococcus aureus Cowan; SMAD — mothers against decapentaplegic, homolog of; TFE3 — transcription factor binding to immunoglobulin heavy constant mu enhancer 3 binding to AGAC is sufficient
Summary
The role of the TGF-SMAD signalling pathway in the etiopathogenesis of severe asthma
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