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Pulmonary fibrosis distal airway epithelia are dynamically and structurally dysfunctional

ABSTRACT: To identify genes regulating the jamming transition in healthy distal airway epithelia compared to the dysregulated state in idiopathic pulmonary fibrosis epithelia (IPF) we analyzed RNA from three (3) healthy and four (4) IPF patient cells grown at air-liquid-interface (ALI). This bulk analysis of 3 timepointes (days 4, 8, and 14 of ALI) spanning the jamming transition revealed an enrichment for ERBB- and YAP-related genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE176001 | GEO | 2021/07/01

REPOSITORIES: GEO

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Pulmonary fibrosis distal airway epithelia are dynamically and structurally dysfunctional.

Project description:The airway epithelium serves as the interface between the host and external environment. In many chronic lung diseases, the airway is the site of substantial remodeling after injury. While, idiopathic pulmonary fibrosis (IPF) has traditionally been considered a disease of the alveolus and lung matrix, the dominant environmental (cigarette smoking) and genetic (gain of function MUC5B promoter variant) risk factor primarily affect the distal airway epithelium. Moreover, airway-specific pathogenic features of IPF include bronchiolization of the distal airspace with abnormal airway cell-types and honeycomb cystic terminal airway-like structures with concurrent loss of terminal bronchioles in regions of minimal fibrosis. However, the pathogenic role of the airway epithelium in IPF is unknown. Combining biophysical, genetic, and signaling analyses of primary airway epithelial cells, we demonstrate that healthy and IPF airway epithelia are biophysically distinct, identifying pathologic activation of the ERBB-YAP axis as a specific and modifiable driver of prolongation of the unjammed-to-jammed transition in IPF epithelia. Furthermore, we demonstrate that this biophysical state and signaling axis correlates with epithelial-driven activation of the underlying mesenchyme. Our data illustrate the active mechanisms regulating airway epithelial-driven fibrosis and identify targets to modulate disease progression.

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