Anti-interleukin-33 inhibits cigarette smoke-induced lung inflammation in mice

Authors

  • Chuan Qiu,

    1. Department of Immunology, Medical School of Ningbo University, Ningbo, China
    2. Institute of Inflammation and Immune Diseases, Shantou University Medical College, Shantou, China
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  • Yan Li,

    1. Department of Immunology, Medical School of Ningbo University, Ningbo, China
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  • Mingcai Li,

    Corresponding author
    1. Institute of Inflammation and Immune Diseases, Shantou University Medical College, Shantou, China
    • Department of Immunology, Medical School of Ningbo University, Ningbo, China
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  • Min Li,

    1. Department of Immunology, Medical School of Ningbo University, Ningbo, China
    2. Institute of Inflammation and Immune Diseases, Shantou University Medical College, Shantou, China
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  • Xiaojin Liu,

    1. Institute of Inflammation and Immune Diseases, Shantou University Medical College, Shantou, China
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  • Charles McSharry,

    1. Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK
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  • Damo Xu

    Corresponding author
    1. Institute of Inflammation and Immune Diseases, Shantou University Medical College, Shantou, China
    2. Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK
    • Department of Immunology, Medical School of Ningbo University, Ningbo, China
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Correspondence: Mingcai Li, Department of Immunology, Medical School of Ningbo University, 818 Fenghua Road, Ningbo 315211, China. Email: limingcai@nbu.edu.cn and Damo Xu, Institute of Infection, Immunity and Inflammation, 120 University Place, University of Glasgow, Glasgow, G12 8TA, UK. Email: Damo.Xu@glasgow.ac.uk

Senior authors: Mingcai Li and Damo Xu

Summary

The 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.

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