Increased IL-33 expression in chronic obstructive pulmonary disease

• Published in: American journal of physiology. Lung cellular and molecular physiology Vol. 308; no. 7; pp. L619 - L627
• Main Authors: Xia, Jie, Zhao, Junling, Shang, Jin, Li, Miao, Zeng, Zhilin, Zhao, Jianping, Wang, Jianmiao, Xu, Yongjian, Xie, Jungang
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.04.2015
• Subjects: Aged; Case-Control Studies; Cells, Cultured; Chronic obstructive pulmonary disease; Cytokines; Female; Flow cytometry; Genetic Association Studies; Humans; Interleukin-1 Receptor Accessory Protein - blood; Interleukin-1 Receptor-Like 1 Protein; Interleukin-33; Interleukins - blood; Interleukins - genetics; Lipopolysaccharides - pharmacology; Lung - metabolism; Lymphocytes; Lymphocytes - immunology; Lymphocytes - metabolism; Male; Middle Aged; Neutrophils - immunology; Neutrophils - metabolism; Pathogenesis; Polymorphism, Single Nucleotide; Pulmonary Disease, Chronic Obstructive - blood; Pulmonary Disease, Chronic Obstructive - genetics; Receptors, Cell Surface - blood; Toll-Like Receptor 4 - genetics; Up-Regulation; peripheral blood lymphocytes; human bronchial epithelial cells; interleukin-33; chronic obstructive pulmonary disease
• DOI: 10.1152/ajplung.00305.2014
• ISSN: 1040-0605; 1522-1504

Chronic obstructive pulmonary disease (COPD) is an inflammatory lung disease characterized by inflammatory cell activation and the release of inflammatory mediators. Interleukin-33 (IL-33) plays a critical role in various inflammatory and immunological pathologies, but evidence for its role in COPD is lacking. This study aimed to investigate the expression of IL-33 in COPD and to determine whether IL-33 participates in the initiation and progression of COPD. Levels of serum IL-33 and its receptors were measured by ELISA, and serum levels of IL-33, ST2, and IL-1 receptor accessory protein were elevated in patients with COPD compared with control subjects. Flow cytometry analysis further demonstrated an increase in peripheral blood lymphocytes (PBLs) expressing IL-33 in patients with COPD. Immunofluorescence analysis revealed that the main cellular source of IL-33 in lung tissue was human bronchial epithelial cells (HBEs). Cigarette smoke extract and lipopolysaccharide could enhance the ability of PBLs and HBEs to express IL-33. Furthermore, PBLs from patients with COPD showed greater IL-33 release in response to the stimulus. Collectively, these findings suggest that IL-33 expression levels are increased in COPD and related to airway and systemic inflammation. Therefore, IL-33 might contribute to the pathogenesis and progression of this disease.