P07 - Susceptibility and response of primary human bronchial epithelial cells to environmental agents
Bronchial epithelial cells play an important role in disease etiology of both idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD). Smoking is a common risk factor for IPF and COPD, but it is not understood which mechanisms lead to the development of one disease rather than the other in response to cigarette smoke. This project aims to elucidate the differences between IPF- and COPD-derived primary bronchial epithelial cells in terms of susceptibility and response to cigarette smoke. We will use state-of-the art proteome, secretome, and gene promoter methylation analysis to generate mechanistic hypotheses for functional validation in relevant animal models and patient samples.
Project-related publications:
1. Knüppel L, Ishikawa Y, Aichler M, Heinzelmann K, Hatz R, Behr J, Walch A, Bächinger HP, Eickelberg O, Staab-Weijnitz CA. A Novel Antifibrotic Mechanism of Nintedanib and Pirfenidone. Inhibition of Collagen Fibril Assembly. Am J Respir Cell Mol Biol 2017; 57(1):77-90
2. Staab-Weijnitz CA, Fernandez IE, Knüppel L, Maul J, Heinzelmann K, Juan-Guardela BM, Hennen E, Preissler G, Winter H, Neurohr C, Hatz R, Lindner M, Behr J, Kaminski N, Eickelberg O. FK506-Binding Protein 10, a Potential Novel Drug Target for Idiopathic Pulmonary Fibrosis. Am J Respir Crit Care Med 2015; 192:455-467
3. Schamberger AC, Schiller HB, Fernandez IE, Sterclova M, Heinzelmann K, Hennen E, Hatz R, Behr J, Vasakova M, Mann M, Eickelberg O, Staab-Weijnitz CA. Glutathione peroxidase 3 localizes to the epithelial lining fluid and the extracellular matrix in interstitial lung disease. Sci Rep 2016; 6: 29952
4. Schamberger AC, Staab-Weijnitz CA, Mise-Racek N, Eickelberg O. Cigarette smoke alters primary human bronchial epithelial cell differentiation at the air-liquid interface. Sci Rep 2015; 5: 8163