Table 1.
Workshop Recommendations
| Epidemiological and clinical research |
| • Undertake longitudinal studies in broad populations to better define the prevalence of ACO and its course. |
| • Phenotype asthma and COPD with respect to specific cellular or biologic processes. |
| • Clinical trials should include and stratify smoking patients with asthma, especially for studies involving targeted therapies. |
| • Assess inhaled corticosteroid efficacy in patients who have asthma and persistent airflow limitation. |
| • Investigate which COPD subgroup(s) has favorable response to ICS. |
| • Determine when fixed airflow limitation develops (i.e., childhood, adulthood, or both) and what drives its development. |
| • Assess structural and functional airway disease using imaging and investigate how these features relate to diagnosis and responsiveness to interventions in asthma, ACO, or COPD. |
| • Study the applicability of imaging measures as surrogate endpoints in clinical trials. |
| • Perform MRI studies of the nature of airway obstruction in ACO. |
| • Link respiratory health with genetic ancestry and the effects of acculturation to better understand respiratory health in underrepresented populations. |
| • Consider the effects of social determinants of health, both individually and at the population level, and socioeconomic inequality in driving asthma, COPD, and ACO. |
| • Understand the role of comorbidities in ACO. |
| Basic and applied research |
| • Identify specific gene signatures in lung cells that are associated with “fixed” airflow limitation, neutrophilia, and smoking. |
| • Conduct mechanistic studies to better understand the interplay of inflammatory and remodeling pathways and their functional impact in ACO. |
| • Investigate the role of RSV and other respiratory viral infections in airflow limitation. |
| • Address the role of respiratory viral infections in initiating the type-2 immune response and mucus cell metaplasia. |
| • Use multilevel systems biology approaches (including genetics, gene expression, and proteomics) to provide insights into disease mechanisms underlying ACO and inform phenotyping. |
| • Understand the utility and role of mucin subtypes (especially MUC5AC and MUC5B) in defining and contributing to airway disease in asthma, COPD, and ACO. |
| • Determine the influence of host genetics and the environment on the development of biological phenotypes. |
| • Investigate the stability of phenotypes of airway disease. |
| • Define whether these phenotypes confer a different natural history/future risk and response to therapies. |
| • Discover and develop new and more precise therapeutics for the airway disease in ACO. |
Definition of abbreviations: ACO = asthma–chronic obstructive pulmonary disease overlap; COPD = chronic obstructive pulmonary disease; ICS = inhaled corticosteroids; MRI = magnetic resonance imaging; RSV = respiratory syncytial virus.