Chronic obstructive pulmonary disease subpopulations and phenotyping

Abstract

The diagnosis and treatment of chronic obstructive pulmonary disease (COPD) has been based largely on a one-size-fits-all approach. Diagnosis of COPD is based on meeting the physiologic criteria of fixed obstruction in forced expiratory flows and treatment focus on symptomatic relief, with limited effect on overall prognosis. However, patients with COPD have distinct features that determine very different evolutions of the disease. In this review we highlight distinct subgroups of COPD characterized by unique pathophysiologic derangements, response to treatment, and disease progression. It is likely that identification of subgroups of COPD will lead to discovery of much needed disease-modifying therapeutic approaches. We argue that a precision approach that integrates multiple dimensions (clinical, physiologic, imaging, and endotyping) is needed to move the field forward in the treatment of this disease.

Molecular and Cellular Mechanisms Responsible for Beneficial Effects of Mesenchymal Stem Cell-Derived Product “Exo-d-MAPPS” in Attenuation of Chronic Airway Inflammation

“…Hallmarks of early stages of COPD include remodeling of small airways induced by persistently activated innate immune cells (alveolar macrophages, neutrophils, natural killer (NK), and DCs), while severe stages of COPD are characterized by the development of lung lymphoid follicles due to the enhanced activation of CD8+ cytotoxic T lymphocytes (CTLs) and CD4+ T helper cells and their crosstalk with B cells [4][5][6][7][8]. Continuous activation of resident and lunginfiltrated immune cells results in structural and functional changes in the inflamed lungs, including the narrowing of small airways, mucus hyperproduction, cilia dysfunction, and destruction of the lung parenchyma [9]. Accordingly, COPD is manifested by persistent and progressive breathlessness (usually worse during physical activities), chronic cough, regular production of sputum (in three or more months during two consecutive years), wheeze, and chest tightness (as signs of severe COPD) [9].…”

“…Continuous activation of resident and lunginfiltrated immune cells results in structural and functional changes in the inflamed lungs, including the narrowing of small airways, mucus hyperproduction, cilia dysfunction, and destruction of the lung parenchyma [9]. Accordingly, COPD is manifested by persistent and progressive breathlessness (usually worse during physical activities), chronic cough, regular production of sputum (in three or more months during two consecutive years), wheeze, and chest tightness (as signs of severe COPD) [9].…”

New insights into the function, development, and plasticity of type 2 innate lymphoid cells

“…Tobacco smoking is the predominant cause of COPD, however, air pollution and genetic predispositions may also play a role. COPD is usually characterized by neutrophilia and type 1 inflammatory responses . Recent studies demonstrate changes in lung ILC distribution in COPD pathology.…”

Novel insights into the effects of cigarette smoke on the airway epithelial surface—lessons learned at the European Respiratory Society International Congress 2018 in Paris

“…The latter is defined as a permanent enlargement of airspaces due to a destruction of the alveolar wall, which results in reduced surface for gas exchange, hypoxemia and a significant decrease of lung tissue elastance. In summary, all these factors favor air trapping and thereby account negatively to the prognosis of COPD (35). The complex processes involving emphysema development have partially been attributed to an increased synthesis and release of reactive oxygen species (ROS), and reactive nitrogen species (RNS) and impaired anti-oxidant defense upon CS-exposure (36).…”