Interaction of TGF-β with Immune Cells in Airway Disease

Benjamin      Moore; Richard   F.   Murphy; Devendra   K.   Agrawal

doi:10.2174/156652408785160943

Abstract

Asthma, chronic obstructive pulmonary disorder (COPD), and cystic fibrosis (CF), chronic diseases of the airways, are characterized by symptoms such as inflammation of the lung tissue, mucus hypersecretion, constriction of the airways, and excessive fibrosis of airway tissue. Transforming growth factor (TGF)-β, a cytokine that affects many different cell processes, has an important role in the lungs of patients with some of these chronic airway diseases, especially with respect to airway remodeling. Eosinophils can be activated by and are a major source of TGF-β in asthma. The action of TGF-β also shows associations with other cell types, such as T cells and neutrophils, which are involved in the pathogenesis of asthma. TGF-β can perpetuate the pathogenesis of COPD and CF, as well, through its induction of inflammation via release from and action on different cells. The intracellular signaling induced by TGF-β in various cell types has been elucidated and may point to mechanisms of action by TGF-β on different structural or immune cells in these airway diseases. Some possible treatments, especially that prevent the deleterious airway changes induced by the action of either eosinophils or TGF-β in asthma, have been investigated. TGF-β-induced signaling pathways, especially those in different cell types in asthma, COPD, or CF, may provide potential therapeutic targets for the treatment of some of the most devastating airway diseases.

Keywords: Airway remodeling, asthma, COPD, cystic fibrosis, eosinophil, inflammation, TGF-β

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