Association of serum interleukin-27 with the exacerbation of chronic obstructive pulmonary disease

Authors

  • Takashi Angata,

    Corresponding author
    1. Systems Glycobiology Research Group, Global Research Cluster, Saitama, Japan
    2. Institute of Biological Chemistry, Academia Sinica, Taipei, Taiwan
    • Correspondence

      Takashi Angata, Institute of Biological Chemistry, Academia Sinica, 128 Section 2, Academia Road, Nankang District, Taipei 11529, Taiwan.

      Tel: +886-2-2785-5696 ext. 6140

      Fax: +886-2-2788-9759

      E-mail: angata@gate.sinica.edu.tw

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    • T. A. and T. I. contributed equally to this work.
  • Takeo Ishii,

    1. Respiratory Care Clinic, Nippon Medical School, Tokyo, Japan
    2. Division of Pulmonary Medicine, Infectious Diseases and Oncology, Department of Internal Medicine, Nippon Medical School, Tokyo, Japan
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    • T. A. and T. I. contributed equally to this work.
  • Congxiao Gao,

    1. Systems Glycobiology Research Group, Global Research Cluster, Saitama, Japan
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  • Kazuaki Ohtsubo,

    1. Systems Glycobiology Research Group, Global Research Cluster, Saitama, Japan
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  • Shinobu Kitazume,

    1. Systems Glycobiology Research Group, Global Research Cluster, Saitama, Japan
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  • Akihiko Gemma,

    1. Division of Pulmonary Medicine, Infectious Diseases and Oncology, Department of Internal Medicine, Nippon Medical School, Tokyo, Japan
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  • Kozui Kida,

    1. Respiratory Care Clinic, Nippon Medical School, Tokyo, Japan
    2. Division of Pulmonary Medicine, Infectious Diseases and Oncology, Department of Internal Medicine, Nippon Medical School, Tokyo, Japan
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  • Naoyuki Taniguchi

    1. Systems Glycobiology Research Group, Global Research Cluster, Saitama, Japan
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  • This work was supported by Global COE program “Frontier Biomedical Science Underlying Organelle Network” from Ministry of Education, Culture, Sports, Science and Technology of Japan (T. A. and N. T.) and the Advanced Research for Medical Products Mining Programme of the National Institute of Biomedical Innovation (NIBIO), Japan (K. K. and N. T.).

Abstract

We have previously demonstrated that chronic obstructive pulmonary disease (COPD) patients who do not have Siglec-14 are less prone to exacerbation of the disease. Siglec-14 is a myeloid cell protein that recognizes bacteria and triggers inflammatory responses. Therefore, soluble mediators secreted by myeloid cells responding to Siglec-14 engagement could be involved in the pathogenesis of exacerbation and could potentially be utilized as biomarkers of exacerbation. To find out, we sought genes specifically induced in Siglec-14+ myeloid cells and evaluated their utility as biomarkers of COPD exacerbation. Using DNA microarray, we compared gene expression levels in Siglec-14+ and control myeloid cell lines stimulated with or without nontypeable Haemophilus influenzae to select genes that were specifically induced in Siglec-14+ cells. The expressions of several cytokine and chemokine genes were specifically induced in Siglec-14+ cells. The concentrations of seven gene products were analyzed by multiplex bead array assays in paired COPD patient sera (n = 39) collected during exacerbation and stable disease states. Those gene products that increased during exacerbation were further tested using an independent set (n = 32) of paired patient sera. Serum concentration of interleukin-27 (IL-27) was elevated during exacerbation (discovery set: P = 0.0472; verification set: P = 0.0428; combined: P = 0.0104; one-sided Wilcoxon matched-pairs signed-rank test), particularly in exacerbations accompanied with sputum purulence and in exacerbations lasting more than a week. We concluded that IL-27 might be mechanistically involved in the exacerbation of COPD and could potentially serve as a systemic biomarker of exacerbation.

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