COPD and Asthma – Definitely two distinct diseases

Abstract

Asthma and chronic obstructive pulmonary disease (COPD) are chronic respiratory diseases characterized by obstruction to expiratory airflow with a high prevalence worldwide. Although they share clinical manifestations, pathophysiological mechanisms, and can coexist in the same patient, they are distinct entities not only in their origin but also in relation to their response to treatment. This article aims to review the immunoinflammatory mechanisms, from the epithelial barrier to the lung parenchyma, in order to substantiate this distinction. From a pathophysiological point of view, asthma is predominantly characterized by a type 2 (T2) inflammatory response. The activated epithelium releases alarmins (mainly TSLP and IL-33), stimulating the production of cytokines (IL-4, IL-5, IL-13) that lead to bronchial hyperresponsiveness and airway remodeling. In COPD, the primary inflammatory pathway is Th1/Th17 with neutrophilic recruitment, oxidative stress, and protease/antiprotease imbalance, resulting in parenchymal destruction and bronchial thickening. However, 20-40% of COPD patients may present with concomitant T2 inflammation characteristics. Clinically, these differences in inflammatory pathways define therapy: asthma has inhaled corticosteroids as a mandatory first-line treatment, while COPD is based on bronchodilators, reserving corticosteroids for exacerbating and/or T2 profiles. The recognition of phenotypes and endotypes, through biomarkers, allows us to abandon the historical view that only asthma has T2 inflammation, recognizing the heterogeneity of both diseases and moving towards precision medicine. Correctly identifying the underlying mechanisms and treatable traits is essential for the application of targeted therapies such as immunobiologics, ensuring improved prognosis and symptom control for both asthma and COPD.