title: Association of serum interleukin-27 with the exacerbation of chronic obstructive pulmonary disease.
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.
authors.affiliation: Systems Glycobiology Research Group, Global Research Cluster, Wako, Saitama, Japan Institute of Biological Chemistry, Academia Sinica, Taipei, Taiwan.
authors.forename: Takashi
authors.initials: T
authors.lastname: Angata
authors.affiliation: Respiratory Care Clinic, Nippon Medical School, Tokyo, Japan Division of Pulmonary Medicine, Infectious Diseases and Oncology, Department of Internal Medicine, Nippon Medical School, Tokyo, Japan.
authors.forename: Takeo
authors.initials: T
authors.lastname: Ishii
authors.affiliation: Systems Glycobiology Research Group, Global Research Cluster, Wako, Saitama, Japan.
authors.forename: Congxiao
authors.initials: C
authors.lastname: Gao
authors.affiliation: Systems Glycobiology Research Group, Global Research Cluster, Wako, Saitama, Japan.
authors.forename: Kazuaki
authors.initials: K
authors.lastname: Ohtsubo
authors.affiliation: Systems Glycobiology Research Group, Global Research Cluster, Wako, Saitama, Japan.
authors.forename: Shinobu
authors.initials: S
authors.lastname: Kitazume
authors.affiliation: Division of Pulmonary Medicine, Infectious Diseases and Oncology, Department of Internal Medicine, Nippon Medical School, Tokyo, Japan.
authors.forename: Akihiko
authors.initials: A
authors.lastname: Gemma
authors.affiliation: Respiratory Care Clinic, Nippon Medical School, Tokyo, Japan Division of Pulmonary Medicine, Infectious Diseases and Oncology, Department of Internal Medicine, Nippon Medical School, Tokyo, Japan.
authors.forename: Kozui
authors.initials: K
authors.lastname: Kida
authors.affiliation: Systems Glycobiology Research Group, Global Research Cluster, Wako, Saitama, Japan.
authors.forename: Naoyuki
authors.initials: N
authors.lastname: Taniguchi
keywords: Adaptive immunity; Siglec‐14; biomarkers; inflammation; innate immunity