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Periostin may play a protective role in the development of eosinophilic chronic rhinosinusitis with nasal polyps in a mouse model

Authors

  • Sang-Wook Kim MD,

    1. Institute of Health Sciences, Gyeongsang National University Hospital, Jinju
    2. Department of Otorhinolaryngology, Gyeongsang National University Hospital, Jinju
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  • Jin Hyun Kim PhD,

    1. Institute of Health Sciences, Gyeongsang National University Hospital, Jinju
    2. Clinical Research Institute, Gyeongsang National University Hospital, Jinju
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  • Myeong Hee Jung MS,

    1. Clinical Research Institute, Gyeongsang National University Hospital, Jinju
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  • Dong Gu Hur MD,

    1. Institute of Health Sciences, Gyeongsang National University Hospital, Jinju
    2. Department of Otorhinolaryngology, Gyeongsang National University Hospital, Jinju
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  • Hong-Kyoung Lee MD,

    1. Department of Otorhinolaryngology, Gyeongsang National University Hospital, Jinju
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  • Sea-Yuong Jeon MD,

    1. Institute of Health Sciences, Gyeongsang National University Hospital, Jinju
    2. Department of Otorhinolaryngology, Gyeongsang National University Hospital, Jinju
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  • Dae Woo Kim MD

    Corresponding author
    1. Department of Otorhinolaryngology, Seoul National University College of Medicine, Boramae Medical Center, Seoul, Korea
    • Institute of Health Sciences, Gyeongsang National University Hospital, Jinju
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  • This study was supported by a grant of the Korean Health Technology R&D Project, Ministry of Health and Welfare, Republic of Korea (A110814).

  • The authors have no other funding, financial relationships, or conflicts of interest to disclose.

Send correspondence to Dae Woo Kim, MD, Department of Otorhinolaryngology, Seoul National University College of Medicine, Boramae Medical Center, 425 Shindaebang 2-dong, Dongjak-gu, Seoul, 156-707, South Korea. E-mail: kicubi@paran.com

Abstract

Objectives/Hypothesis

Several genes have been reported to be upregulated in human nasal polyps in previous genetic analyses. Among these genes, periostin is known to be overexpressed in nasal polyps obtained from aspirin-sensitive patients. Using periostin-null mice, we investigated the role of periostin in a murine model of eosinophilic rhinosinusitis with nasal polyps.

Study Design

Animal study.

Methods

Eosinophilic rhinosinusitis was induced in both periostin-null and wild-type mice according to previously established protocols. In brief, ovalbumin (OVA) was used for sensitization and prolonged intranasal stimulation. Staphylococcus aureus enterotoxin B was applied intranasally to develop polyplike lesions. To examine the inflammation and mucosal lesions, hematoxylin and eosin, Sirius red, and Giemsa staining were performed.

Results

There was no definite difference in the maximal mucosal thickness between periostin-null and wild-type mice. In contrast, some parameters of inflammation, including the number of polyplike lesions and mast cells, were aggravated in the periostin-null mice compared to wild type. Eosinophilic infiltration was aggravated in the OVA-stimulated periostin-null mice, compared to OVA-stimulated wild-type mice, whereas there was no apparent difference between wild-type and periostin-null mice challenged with additional S aureus enterotoxin B.

Conclusions

The loss of periostin appears to enhance polyplike lesion formation and mast cell infiltration in a mouse model of eosinophilic rhinosinusitis with nasal polyps.

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