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These studies suggest that COPD and asthma are distinct but overlapping respiratory diseases with different immune cell involvement, genetic signatures, and inflammation patterns, and that Asthma-COPD overlap syndrome (ACOS) affects a significant portion of patients, leading to worse symptoms and quality of life.
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Chronic Obstructive Pulmonary Disease (COPD) is a progressive lung disease characterized by chronic inflammation and airflow limitation. The primary cause of COPD is long-term exposure to harmful substances, most commonly cigarette smoke, which leads to damage in the airways and lung parenchyma. COPD is marked by symptoms such as chronic bronchitis and emphysema, which result in persistent respiratory symptoms and airflow obstruction. The inflammatory response in COPD predominantly involves neutrophils, macrophages, and lymphocytes, with eosinophils playing a minor role except during exacerbations.
Asthma is a chronic inflammatory disease of the airways that leads to episodes of wheezing, breathlessness, chest tightness, and coughing. It is characterized by airway hyperresponsiveness (AHR) and variable airflow obstruction, which is often reversible either spontaneously or with treatment. The inflammation in asthma primarily involves eosinophils, mast cells, and T helper type 2 (Th2) cells, which contribute to the characteristic symptoms and response to therapy. Asthma typically has an early onset and is often associated with other allergic conditions.
The inflammatory profiles of COPD and asthma are distinct, with different patterns of inflammatory cells and mediators involved. In asthma, the inflammation is largely driven by eosinophils and Th2 cells, whereas in COPD, the inflammation is predominantly neutrophilic and involves macrophages and lymphocytes . These differences in cellular and molecular mechanisms account for the variations in clinical manifestations and responses to therapy between the two diseases.
Asthma-COPD Overlap (ACO) refers to a condition where patients exhibit features of both asthma and COPD. This overlap is recognized in patients who have persistent airflow limitation with characteristics of both diseases, such as a history of asthma and significant smoking history . ACO is associated with increased morbidity, poorer quality of life, and a higher risk of exacerbations compared to having either disease alone . The inflammatory profile in ACO can include eosinophilic, neutrophilic, or mixed patterns, reflecting the contributions of both asthma and COPD mechanisms.
The recognition of ACO has important implications for treatment, as patients may benefit from therapies targeting both eosinophilic and neutrophilic inflammation. For instance, corticosteroids, which are effective in asthma, may also benefit a subset of COPD patients with Th2-high inflammation. However, there is a need for more research to develop targeted treatments for ACO and to better understand the underlying mechanisms.
COPD and asthma are both chronic obstructive airway diseases with distinct inflammatory profiles and clinical features. While COPD is primarily driven by neutrophilic inflammation due to smoking, asthma is characterized by eosinophilic inflammation and airway hyperresponsiveness. The overlap between these diseases, known as ACO, presents a unique challenge in diagnosis and treatment, necessitating a multidimensional approach to manage the heterogeneous nature of these conditions effectively. Further research is essential to develop personalized therapies that address the specific inflammatory patterns in ACO.
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