Abstract 19020: ABCG1 Regulates Pulmonary Surfactant Homeostasis and the Lung Microbiome
Chronic respiratory diseases are the 3rd leading cause of death, and individuals suffering from respiratory distress are at risk for cardiovascular complications. Changes in the commensal bacteria in the lung have been associated with the development of chronic lung conditions including asthma, cystic fibrosis, chronic obstructive pulmonary disease (COPD), and pulmonary fibrosis. The lung is a dynamic environment, constantly subject to influx of debris and microbes. The clearance of pathogens and adaptation to changes in commensal flora are mediated by innate and acquired immune responses that minimize inflammation and maintain pulmonary homeostasis. Surfactant proteins are essential for the structure and function of pulmonary surfactant, produced solely by pulmonary type 2 cells, and have their own intrinsic innate immune properties. The ATP Binding Cassette Transporter G1 (ABCG1) is highly expressed in pulmonary type 2 cells, alveolar macrophages and immune cells. We have recently demonstrated that ABCG1 regulates pulmonary B cell and natural antibody homeostasis. Here we show that mice lacking ABCG1 specifically in pulmonary type 2 cells have altered lamellar body and surfactant homeostasis. Additionally, we show that mice lacking ABCG1 have disturbances in the commensal bacteria that populate the lungs. Abcg1-/- mice may represent a novel model in which to study the interaction between pulmonary surfactant metabolism, pulmonary innate immune responses and the lung microbiome.
Author Disclosures: T.Q. de Aguiar Vallim: None. A. Baldan: None. J. Cheng: None. C. Goulbourne: None. E. Org: None. A.J. Lusis: None. E.J. Tarling: None.
- © 2015 by American Heart Association, Inc.