Eosinophilic and Neutrophilic Airway Inflammation in the Phenotyping of Mild-to-Moderate Asthma and Chronic Obstructive Pulmonary Disease

Abstract

Asthma and chronic obstructive pulmonary disease (COPD) are heterogeneous diseases with different inflammatory phenotypes. Various inflammatory mediators play a role in these diseases. The aim of this study was to analyze the neutrophilic and eosinophilic airway and systemic inflammation as the phenotypic characterization of patients with asthma and COPD. Twenty-four patients with asthma and 33 patients with COPD were enrolled in the study. All the patients were in mild-to-moderate stage of disease, and none of them were treated with inhaled corticosteroids. Concentrations of IL-6, neutrophil elastase (NE), matrix metalloproteinase 9 (MMP-9), eosinophil cationic protein (ECP), and IL-33 and IL-17 in serum and induced sputum (IS) were measured by enzyme-linked immunosorbent assay (ELISA). The cellular composition of blood and IS was evaluated. Hierarchical clustering of patients was performed for the combination of selected clinical features and mediators. Asthma and COPD can be differentiated based on eosinophilic/neutrophilic systemic or airway inflammation with unsatisfactory efficiency. Hierarchical clustering of patients based on blood eosinophil percentage and clinical data revealed two asthma clusters differing in the number of positive skin prick tests and one COPD cluster with two subclusters characterized by low and high blood eosinophil concentrations. Clustering of patients according to IS measurements and clinical data showed two main clusters: pure asthma characterized by high eosinophil/atopy status and mixed asthma and COPD cluster with low eosinophil/atopy status. The neutrophilic phenotype of COPD was associated with more severe airway obstruction and hyperinflation.

Clinical and inflammatory phenotyping by breathomics in chronic airway diseases irrespective of the diagnostic label

“…This study captured clusters based on breathomics that were not predominantly driven by diagnosis but were instead driven by clinical/inflammatory characteristics. Most of these driving factors are commonly identified when attempting to phenotype asthma and/or COPD patients [25][26][27][28][29][30]. Cluster 1 found in our study contains predominantly females with a high BMI, no inflammation and high symptom scores.…”

Different expression about induced sputum cell sorting in the two main types of chronic obstructive pulmonary disease

“…A significant correlation was found between number of sputum eosinophils (A phenotype) and the type of dyspnea group (D phenotype) (0.535; P ≤ .001). Percentage sputum eosinophil count was predictive of dyspnea (D phenotype) COPD with AUC of 0.831 (95% CI 0.77–0.89; P ≤ .001) (Figure A), and in some studies, the correlation has been close …”

Environmental pollutants damage airway epithelial cell cilia: Implications for the prevention of obstructive lung diseases

“…These can be further divided according to the form of pollutant: gaseous pollutants, liquid pollutants, and solid pollutants; and according to the nature of the pollutant: chemical contaminants, physical pollutants, and biological contaminants . The harm of environmental pollutants to the human body is mainly reflected in respiratory mucosa damage and obstructive pulmonary disease because the respiratory tract is the first thing affected by environmental exposure . Several studies have shown that in environments with air pollution, the cilia in the human respiratory tract become shorter or are missing, which affects their ability to clear the respiratory tract.…”

“…39 The harm of environmental pollutants to the human body is mainly reflected in respiratory mucosa damage and obstructive pulmonary disease because the respiratory tract is the first thing affected by environmental exposure. 40 Several studies have shown that in environments with air pollution, the cilia in the human respiratory tract become shorter or are missing, which affects their ability to clear the respiratory tract. For example, when experimental animals were exposed to higher concentrations of ozone (4 ppm), it was observed that the vesicles of the ciliated membrane and the structure of the tracheal cilia were damaged.…”