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Expression of IL-33 and its receptor ST2 in chronic rhinosinusitis with nasal polyps

Authors

  • Shintaro Baba MD,

    Corresponding author
    1. Department of Otolaryngology, Faculty of Medicine, The University of Tokyo, Bunkyo-ku
    • Send correspondence to Shintaro Baba, MD, Department of Otolaryngology, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113–8655, Japan. E-mail: sbaba-tky@umin.ac.jp

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  • Kenji Kondo MD, PhD,

    1. Department of Otolaryngology, Faculty of Medicine, The University of Tokyo, Bunkyo-ku
    2. Division of Respiratory Medicine and Allergology, Department of Medicine, Teikyo University School of Medicine, Itabashi-ku
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  • Kaori Kanaya MD,

  • Keigo Suzukawa MD, PhD,

    1. Department of Otolaryngology, Faculty of Medicine, The University of Tokyo, Bunkyo-ku
    2. Division of Respiratory Medicine and Allergology, Department of Medicine, Teikyo University School of Medicine, Itabashi-ku
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  • Munetaka Ushio MD, PhD,

    1. Department of Otolaryngology, Faculty of Medicine, The University of Tokyo, Bunkyo-ku
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  • Shinji Urata MD,

    1. Department of Otolaryngology, Faculty of Medicine, The University of Tokyo, Bunkyo-ku
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  • Takahiro Asakage MD, PhD,

    1. Department of Otolaryngology, Faculty of Medicine, The University of Tokyo, Bunkyo-ku
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  • Akinobu Kakigi MD, PhD,

    1. Department of Otolaryngology, Faculty of Medicine, The University of Tokyo, Bunkyo-ku
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  • Maho Suzukawa MD, PhD,

    1. Division of Respiratory Medicine and Allergology, Department of Medicine, Teikyo University School of Medicine, Itabashi-ku
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  • Ken Ohta MD, PhD,

    1. Division of Respiratory Medicine and Allergology, Department of Medicine, Teikyo University School of Medicine, Itabashi-ku
    2. National Hospital Organization Tokyo National Hospital, Kiyose-city, Tokyo, Japan
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  • Tatsuya Yamasoba MD, PhD

    1. Department of Otolaryngology, Faculty of Medicine, The University of Tokyo, Bunkyo-ku
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  • This work was supported by Grants-in-Aid for Young Scientists (B) (Shintaro Baba, MD; Kenji Kondo, MD, PhD; Maho Suzukawa, MD, PhD), a Health and Labour Sciences Research Grant from the Ministry of Health, Labour and Welfare, Japan (Ken Ohta, MD, PhD), and a grant from the Environmental Restoration and Conservation Agency of Japan (Ken Ohta, MD, PhD). Maho Suzukawa, MD, PhD, is supported by a Postdoctoral Fellowship for Research Abroad from the Japan Society for the Promotion of Science. The authors have no additional funding, financial relationships, or conflicts of interest to disclose.

Abstract

Objectives/Hypothesis

Interleukin (IL)−33 is a novel member of the IL-1 cytokine family and a ligand for the orphan IL-1 family receptor ST2. IL-33 induces T helper 2-type inflammatory responses and is considered to play a crucial role in allergic inflammatory reactions such as asthma and atopic dermatitis. However, the role of IL-33 and its receptor ST2 in chronic rhinosinusitis remains unclear.

Study Design

In vitro study.

Methods

The expression patterns of IL-33 and ST2 at both mRNA and protein levels in nasal polyps from eosinophilic chronic rhinosinusitis (ECRS) patients (n = 10) and non-ECRS patients (n = 13), as well as in seemingly normal mucosa of the uncinate processes in patients without sinusitis (control; n = 5), were compared using immunohistochemical staining, enzyme-linked immunosorbent assay, and real-time polymerase chain reactions.

Results

ST2-positive cells in the inflammatory cells in the subepithelial layer were significantly higher in the ECRS group than other groups. The expression of ST2 mRNA in polyps of the ECRS group was significantly increased compared with controls. Many ST2-positive eosinophils were observed in the mucosa of ECRS but not in the mucosa of non-ECRS patients. The expression level of IL-33 mRNA was not significantly different among the three groups.

Conclusions

The current study suggests that IL-33 and its receptor ST2 may play important roles in the pathogenesis of chronic rhinosinusitis, especially in ECRS, through the increased expression of ST2 in eosinophils.

Level of Evidence

N/A. Laryngoscope, 124:E115–E122, 2014

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