Chuan Qiu1,2, Yan Li1, Mingcai Li1,2, Min Li1,2, Xiaojin Liu2, Charles McSharry3, Damo Xu1,3,2
1Department of Immunology Medical School of Ningbo University Ningbo China
2Institute of Inflammation and Immune Diseases, Shantou University Medical College, Shantou, China
3Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK
Tóm tắt
SummaryThe mechanism by which cigarette smoke (CS) causes chronic obstructive pulmonary disease (COPD) is poorly understood. Interleukin‐33 (IL‐33) is a pleiotropic cytokine predominantly expressed in lung tissue and can elicit airway inflammation in naive mice. We tested the hypothesis that IL‐33 is induced by CS and contributes to CS‐mediated airway inflammation in a mouse model of CS‐induced COPD. Groups of mice were exposed to CS three times per day for 4 consecutive days. The expression levels of IL‐33 and ST2 were markedly enhanced in the lung tissue of mice inhaling CS. Exposure to CS also induced neutrophil and macrophage infiltration and expression of inflammatory cytokines (IL‐1β, tumour necrosis factor‐α, IL‐17), chemokines (monocyte chemoattractant protein‐1) and mucin 5, subtypes A and C in the airways. More importantly, all of these CS‐induced pathogenic changes were significantly inhibited by treatment with neutralizing anti‐IL‐33 antibody delivered intranasally. Hence, our results suggest that IL‐33 plays a critical role in CS‐mediated airway inflammation and may be a therapeutic target in CS‐related diseases, including COPD.
