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Oxidative Stress/Inflammation in Pulmonary Disease

Institution: Scripps Research Institute
Investigator(s): William Balch, Ph.D.
Award Cycle: 2012 (Cycle 21) Grant #: 21XT-0070 Award: $409,427
Subject Area: Early Diagnosis/Pathogenesis
Award Type: Exploratory/Developmental Award

Initial Award Abstract

Chronic obstructive pulmonary disease (COPD), often a cigarette smoking-induced severe and progressive lung disease, affects 13.1 million people and is the third leading cause of death in US. Despite its importance, there is no direct cure for COPD, and the mechanisms by which cigarette smoking triggers the disease remain largely unknown. Recently, an exciting new connection was found between COPD and the cigarette-induced dysfunction of the cystic fibrosis transmembrane conductance regulator (CFTR), a protein that when mutated causes the common inherited genetic disease called cystic fibrosis (CF). Similar to people with COPD, CF patients suffer from persistent airway infection and inflammation, mucus hypersecretion, and mucus plugging of the airway.

In this study, we will now explore the possibility that COPD is in fact a cigarette smoking-induced form of CF. We will provide in depth insights into the mechanisms that link cigarette smoking to CFTR dysfunction through analysis of the lung cell response to CS and loss of CFTR function using state-of-the-art genomic and proteomic technologies. Additionally, we will use our well-established high throughput screening strategy to pinpoint the “protein quality control” pathways that are damaged upon cigarette smoke exposure and thereby discover new drug targets against COPD. This study will set the stage for our ultimate goal - discover chemical compounds that can restore lung function via rescuing CS-damaged CFTR function.