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.

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IL-6 and IL-33 are involved in the inflammatory process in obstructive lung diseases. In contrast to IL-6, few data on the expression of IL-33 in different biological samples from asthma and COPD patients are available. The aim was to evaluate the expressions of IL-33 and IL-6 in bronchial mucosa and to compare these expressions with the concentrations of both cytokines in various respiratory samples from patients with mild-to-moderate asthma and COPD. Serum, induced sputum and exhaled breath condensate IL-6 and IL-33 levels, as well as their expression in bronchial mucosa were evaluated in 22 asthma and 33 COPD patients. There were significant differences between bronchial mucosa IL-6, but not IL-33 expression in asthma and COPD. Serum and IS IL-6 concentrations were higher in COPD than in asthma (3.4 vs. 2.02 pg/mL, p = 0.002 and 16.5 vs. 12.7 pg/mL, p = 0.007, respectively); IL-33 levels reached similar values in asthma and COPD in all investigated samples. In both diseases, the lowest levels of IL-6 and IL-33 were found in EBC. EBC levels of both cytokines did not correlate with their expression in other materials. The IL-33 and IL-6 are detectable in serum, IS and EBC not only in asthma but also in COPD patients. In the COPD group, serum and IS IL-6 concentrations were statistically higher than in the asthma group. The tissue expression of IL-33 and IL-33 concentrations in the investigated biological samples were on a comparable level in both diseases. Our findings may suggest that IL-33 activation is a common pathway in asthma and COPD.

124years, further attempts have been made to precisely identify these phenotypes, and this has initiated a search for new reliable biomarkers. Periostin has been found to be a marker for Th2-associated inflammation in patients with asthma. 1This type of inflammation is associated with an increased eosinophil count not only in peripheral blood, but also in bronchoalveolar lavage fluid (BALF).2 Therefore, periostin may be used as a potential predictor of airway eosinophilia. 3IntroductIon Asthma is a chronic inflammatory disease with a complex immunological background. Eosinophils are the main cells involved in asthma-related airway inflammation; however, there is also a significant contribution of neutrophils, lymphocytes, and mast cells. As the type of inflammation has been shown to affect treatment response, determination of asthma inflammatory phenotypes based on the predominant inflammatory cells has been strongly advocated. In recent AbstrActIntroductIon Periostin is considered to be a marker of eosinophilic inflammation in patients with asthma. However, there are no literature data on periostin in patients with chronic obstructive pulmonary disease (COPD).objectIves The aim of the study was to evaluate periostin expression and to compare its concentrations in various materials in patients with mild-to-moderate asthma and COPD, as well as to evaluate the potential association between periostin and clinical features of both diseases. PAtIents And methodsUsing an enzyme-linked immunosorbent assay, we measured periostin concentrations in serum, induced sputum (IS), exhaled breath condensate (EBC), and bronchoalveolar lavage fluid (BALF) as well as periostin expression in bronchial biopsy samples in 24 patients with asthma, 36 patients with COPD, and 12 controls. Correlations between periostin levels in different materials were also analyzed and periostin concentrations were compared between patients with asthma and those with COPD.results Periostin levels were detectable in serum, IS, EBC, and BALF from patients with asthma, COPD, and controls. EBC periostin levels correlated with tissue periostin expression and were significantly higher in asthma than in COPD (P = 0.04). Periostin expression in bronchial mucosa was higher in asthma than in COPD (P <0.001), as well as in asthma and COPD patients compared with controls (P <0.001). No significant correlations between tissue periostin expression and BALF, IS, or serum periostin levels were found. There were no differences in serum, IS, BALF, or EBC periostin concentrations between patients with different phenotypes of both diseases.conclusIons Periostin may be detected not only in serum, IS, and airway tissue samples, but also in EBC and BALF. EBC periostin levels and tissue periostin expression are higher in patients with asthma than in those with COPD. EBC periostin levels may serve as a potential surrogate marker for tissue periostin expression. 125Patients were recruited from an outpatient clinic and included consecutive patients with asthma and COPD who wer...

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Background: Sarcoidosis and idiopathic pulmonary fibrosis (IPF) are two most

Airway epithelium acts as multifunctional site of response in the respiratory tract. Epithelial activity plays an important part in the pathophysiology of obstructive lung disease. In this study, we compare normal human epithelial cells from various levels of the respiratory tract in terms of their reactivity to pro-allergic and pro-inflammatory stimulation. Normal human nasal, bronchial and small airway epithelial cells were stimulated with IL-4 and IL-13. The expressions of the eotaxins IL-6 and CXCL8 were evaluated at the mRNA and protein levels. The effects of pre-treatment with IFN-γ on the cell reactivity were measured, and the responses to TNF-α, LPS and IFN-γ were evaluated. All of the studied primary cells expressed CCL26, IL-6 and IL-8 after IL-4 or IL-13 stimulation. IFN-γ pre-treatment resulted in decreased CCL26 and increased IL-6 expression in the nasal and small airway cells, but this effect was not observed in the bronchial cells. IL-6 and CXCL8 were produced in varying degrees by all of the epithelial primary cells in cultures stimulated with TNF-α, LPS or IFN-γ. We showed that epithelial cells from the various levels of the respiratory tract act in a united way, responding in a similar manner to stimulation with IL-4 and IL-13, showing similar reactivity to TNF-α and LPS, and giving an almost unified response to IFN-γ pre-stimulation.

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