Abstract
BackgroundInterleukin(IL)-33 is an epithelial alarmin important for eosinophil maturation, activation and survival. The aim of this study was to examine the association between IL-33, its receptor expression and airway eosinophilic inflammation in non-atopic COPD.MethodsIL-33 concentrations were measured in exhaled breath condensate (EBC) collected from healthy non-smokers, asthmatics and non-atopic COPD subjects using ELISA. Serum and sputum samples were collected from healthy non-smokers, healthy smokers and non-atopic COPD patients. Based on sputum eosinophil count, COPD subjects were divided into subgroups with airway eosinophilic inflammation (sputum eosinophils > 3%) or without (sputum eosinophils ≤3%). IL-33 and soluble form of IL-33 receptor (sST2) protein concentrations were measured in serum and sputum supernatants using ELISA. ST2 mRNA expression was measured in peripheral mononuclear cells and sputum cells by qPCR. Hemopoietic progenitor cells (HPC) expressing ST2 and intracellular IL-5 were enumerated in blood and induced sputum by means of flow cytometry.ResultsIL-33 levels in EBC were increased in COPD patients to a similar extent as in asthma and correlated with blood eosinophil count. Furthermore, serum and sputum IL-33 levels were higher in COPD subjects with sputum eosinophilia than in those with a sputum eosinophil count ≤3% (p < 0.001 for both). ST2 mRNA was overexpressed in sputum cells obtained from COPD patients with airway eosinophilic inflammation compared to those without sputum eosinophilia (p < 0.01). Similarly, ST2 + IL-5+ HPC numbers were increased in the sputum of COPD patients with airway eosinophilia (p < 0.001).ConclusionsOur results indicate that IL-33 is involved in the development of eosinophilic airway inflammation in non-atopic COPD patients.
Highlights
Interleukin(IL)-33 is an epithelial alarmin important for eosinophil maturation, activation and survival
No significant difference in blood eosinophil counts was observed between Chronic Obstructive Pulmonary Disease (COPD) patients, healthy non-smokers and asthmatic subjects (Table 1)
It was found that 25% of COPD subjects had sputum eosinophilia > 3%
Summary
Interleukin(IL)-33 is an epithelial alarmin important for eosinophil maturation, activation and survival. Non-allergic COPD patients with blood eosinophil counts > 250 cells/μL are characterized by higher airway eosinophil numbers, higher sputum interleukin(IL)-5 and haptoglobin levels, greater CCL20 and CCL24 concentrations in bronchoalveolar lavage (BAL) and more pronounced airway remodeling [8]. Recent evidence has demonstrated that IL-33 precedes IL-5 in regulating eosinophil commitment and is required for eosinophil homeostasis [10]. One such result of IL-33 activity is that activates and augments the maturation of hemopoietic progenitor cells (HPC). HPC are considered to be innate effector cells in allergic asthma [11, 12]: They produce an abundance of pro-inflammatory cytokines and differentiate into mature eosinophils in the process of “in situ hemopoiesis” at sites of inflammation [13]
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