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Overexpression of IL-38 protein in anticancer drug-induced lung injury and acute exacerbation of idiopathic pulmonary fibrosis

  1. Author:
    Tominaga, Masaki
    Okamoto, Masaki
    Kawayama, Tomotaka
    Matsuoka, Masanobu
    Kaieda, Shinjiro
    Sakazaki, Yuki
    Kinoshita, Takashi
    Mori, Daisuke
    Inoue, Akira
    Hoshino, Tomoaki

  2. Author Address

    Department of Medicine 1, Division of Respirology, Neurology and Rheumatology, Kurume University School of Medicine, Kurume 830-0011, Japan. Electronic address: tominaga_masaki@med.kurume-u.ac.jp., Department of Medicine 1, Division of Respirology, Neurology and Rheumatology, Kurume University School of Medicine, Kurume 830-0011, Japan. Electronic address: okamoto_masaki@med.kurume-u.ac.jp., Department of Medicine 1, Division of Respirology, Neurology and Rheumatology, Kurume University School of Medicine, Kurume 830-0011, Japan. Electronic address: kawayama_tomotaka@med.kurume-u.ac.jp., Department of Medicine 1, Division of Respirology, Neurology and Rheumatology, Kurume University School of Medicine, Kurume 830-0011, Japan. Electronic address: matsuoka_masanobu@kurume-u.ac.jp., Department of Medicine 1, Division of Respirology, Neurology and Rheumatology, Kurume University School of Medicine, Kurume 830-0011, Japan. Electronic address: kaieda@med.kurume-u.ac.jp., Department of Medicine 1, Division of Respirology, Neurology and Rheumatology, Kurume University School of Medicine, Kurume 830-0011, Japan. Electronic address: sakazaki@med.kurume-u.ac.jp., Department of Medicine 1, Division of Respirology, Neurology and Rheumatology, Kurume University School of Medicine, Kurume 830-0011, Japan. Electronic address: tkino@kurume-u.ac.jp., Department of Pathology, Saga-Ken Medical Centre Koseikan, Kase 400, Saga 840-8571, Japan. Electronic address: mori-d@koseikan.jp., Department of Respiratory, Tohoku University, Aobaku, Sendai 980-8575, Japan. Electronic address: akinoue@idac.tohoku.ac.jp., Department of Medicine 1, Division of Respirology, Neurology and Rheumatology, Kurume University School of Medicine, Kurume 830-0011, Japan; CIP, NCI-Frederick, NIH, Frederick, MD 21702, United States. Electronic address: hoshino@med.kurume-u.ac.jp.,
    1. Year: 2017
    2. Date: Sep
  2. Journal: Respiratory Investigation
    1. 55
    2. 5
    3. Pages: 293-299
  4. Type of Article: Article
  5. Article Number: 293-299
  1. Abstract:

    Interleukin (IL)-38, a member of the IL-1 family, shows high homology to IL-1 receptor antagonist (IL-1Ra) and IL-36 receptor antagonist (IL-36Ra). Its function in interstitial lung disease (ILD) is still unknown. To determine the expression pattern of IL-38 mRNA, a panel of cDNAs derived from various tissues was analyzed by quantitative real-time PCR. Immunohistochemical reactivity with anti-human IL-38 monoclonal antibody (clone H127C) was evaluated semi-quantitatively in lung tissue samples from 12 patients with idiopathic pulmonary fibrosis/usual interstitial pneumonia (IPF/UIP), 5 with acute exacerbation of IPF, and 10 with anticancer drug-induced ILD (bleomycin in 5 and epidermal growth factor receptor-tyrosine kinase inhibitor in 5). Control lung tissues were obtained from areas of normal lung in 22 lung cancer patients who underwent extirpation surgery. IL-38 transcripts were strongly expressed in the lung, spleen, synoviocytes, and peripheral blood mononuclear cells, and at a lower level in pancreas and muscle. IL-38 protein was not strongly expressed in normal pulmonary alveolar tissues in all 22 control lungs. In contrast, IL-38 was overexpressed in the lungs of 4 of 5 (80%) patients with acute IPF exacerbation and 100% (10/10) of the patients with drug-induced ILD. IL-38 overexpression was limited to hyperplastic type II pneumocytes, which are considered to reflect regenerative change following diffuse alveolar damage in ILD. IL-38 may play an important role in acute and/or chronic inflammation in anticancer drug-induced lung injury and acute exacerbation of IPF. Copyright © 2017 The Japanese Respiratory Society. Published by Elsevier B.V. All rights reserved.

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External Sources

  1. View Full Text
  2. DOI: 10.1016/j.resinv.2017.06.001
  3. PMID: 28942884
  4. View record in Web of Science®
  5. WOS: 000417490000003
  6. PII : S2212-5345(17)30079-5

Library Notes

  1. Fiscal Year: FY2016-2017
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