Organotypic in vitro human airway models can recapitulate aspects of pulmonary fibrosis
Pulmonary fibrosis (PF) is a debilitating, typically fatal condition that may be caused by a variety of factors, including occupational and environmental exposures, drugs such as amiodarone and bleomycin, radiation exposure and genetic predisposition. However, in 20-30% of cases the cause is unknown (i.e. idiopathic pulmonary fibrosis, IPF). Currently approved IPF drugs (pirfenidone, nintedanib) have only had limited efficacy and lung transplantation remains the best treatment option for IPF patients.
Despite intense research, many of the molecular mechanisms involved in the initiation and progression of IPF remain unknown. Current IPF research relies on animal models and ex vivo lung tissues, which are expensive and are not always predictive of clinical trial results. In vitro models produced from immortalized cells also do not adequately replicate IPF.
The goal of the current work is to develop in vitro organotypic, 3D airway models from primary human cells which can be used to study PF.
Pulmonary fibrosis, EpiAlveolar, EpiAirwayFT, Cytokeratin 19, vimentin, Type I Collagen (COL1A1), Fibronectin (Fn), Tumor necrosis factor alpha (TNF-α), TEER, MMP-2, Type III Collagen, E-cadherin, Type I Collagen, α-smooth muscle actin (α-SMA), pro-fibrotic phenotype
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