Abstract
A recent Lancet commission highlighted the significant and increasing burden of chronic obstructive pulmonary disease (COPD) and the need for fundamental changes in the way we think about this disease. Currently, the diagnosis of COPD requires spirometric airway limitation (FEV1/FVC <70%). However, significant lung damage may already have occurred before abnormalities in lung function are identified. Recently, the term pre-COPD has therefore been proposed to refer to individuals without airflow obstruction, but who are at increased risk of subsequently developing COPD based on their symptoms, lung function, or structural abnormalities. Importantly, the pathophysiological mechanisms underlying pre-COPD are largely unknown. Recently, our research group demonstrated a >40% reduction of small airways in pre-COPD patients compared to healthy (smoking) controls, which was similar to established GOLD I COPD. In this project, the cellular and molecular mechanisms underlying structural abnormalities in pre-COPD will be extensively investigated, with a focus on inflammation and epithelial remodeling. A comprehensive strategy will be employed, entailing a thorough transcriptomics investigation and validation at the tissue level, complemented by functional experiments utilizing patient-derived bronchial epithelial cell cultures. Understanding early pathological changes in pre-COPD will ultimately enable earlier and improved diagnosis and therapeutic intervention in (pre-)COPD patients.
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