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IL-32 up-regulation is associated with inflammatory cytokine production in allergic rhinitis

Authors

  • Hyun-Ja Jeong,

    1. Biochip Research Center, Hoseo University, 165, Sechul-ri, Baebang-myun, Asan, Chungnam, 336-795, Republic of Korea
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  • Seung-Youp Shin,

    1. Department of Otolaryngology, College of Medicine, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-gu, Seoul, 130-701, Republic of Korea
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  • Hyun-A Oh,

    1. Department of Pharmacology, College of Oriental Medicine, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-gu, Seoul, 130-701, Republic of Korea
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  • Min-Ho Kim,

    1. High-Enthalpy Plasma Research Center, Chonbuk National University, 664-14, 1 Ga Deokjin-dong, Deokjin-gu, Jeonju, 561-756, Republic of Korea
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  • Joong-Saeng Cho,

    1. Department of Otolaryngology, College of Medicine, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-gu, Seoul, 130-701, Republic of Korea
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  • Hyung-Min Kim

    Corresponding author
    1. Department of Pharmacology, College of Oriental Medicine, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-gu, Seoul, 130-701, Republic of Korea
    • College of Oriental Medicine, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-gu, Seoul, 130-701, South Korea.
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  • No conflicts of interest were declared.

Abstract

IL-32 is a described pro-inflammatory cytokine produced by T lymphocytes, natural killer cells, monocytes, and epithelial cells. However, the specific mechanism of IL-32 on allergic rhinitis (AR) has not been elucidated. Here, we report a significant increase of IL-32 protein and mRNA in the nasal mucosa of AR patients. In addition, in nasal mucosa tissue from AR patients, the level of IL-32 production correlated with inflammation, IL-1β, IL-18, and granulocyte-macrophage colony-stimulating factor (GM-CSF). In an AR animal model, IL-32 significantly increased IgE and inflammatory cytokine levels. IL-32 expression was induced by recombinant human GM-CSF via activation of caspase-1 in eosinophils. In addition, depletion of IL-32 prevents the production of inflammatory cytokines in eosinophils. In conclusion, IL-32 is an important cytokine involved in the inflammation of AR. The regulation of IL-32 expression may form the basis of a new strategy for the treatment of AR. Copyright © 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

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