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Original Research: COPD |

IL-27 Is Elevated in Patients With COPD and Patients With Pulmonary TB and Induces Human Bronchial Epithelial Cells to Produce CXCL10IL-27 in Airways

Ju Cao, PhD; Liping Zhang, PhD; Dairong Li, MD; Fang Xu, MD; Shifeng Huang, PhD; Yu Xiang, MD; Yibing Yin, MD; Guosheng Ren, MD
Author and Funding Information

From the Department of Laboratory Medicine (Drs Cao, Zhang, Huang, and Xiang), the Molecular Oncology and Epigenetics Laboratory (Dr Ren), the Department of Respiratory Disease (Dr Li), and the Department of Emergency and Intensive Care Unit (Dr Xu), The First Affiliated Hospital of Chongqing Medical University; and the Department of Laboratory Medicine (Dr Yin), Chongqing Medical University, Chongqing, China.

Correspondence to: Guosheng Ren, MD, Department of Laboratory Medicine, and Molecular Oncology and Epigenetics Laboratory, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Yuzhong District, Chongqing, 400016, China; e-mail or renguosheng726@163.com


Funding/Support: This study was supported by The National Natural Science Foundation grants of China [No. 81000711].

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2012 American College of Chest Physicians


Chest. 2012;141(1):121-130. doi:10.1378/chest.10-3297
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Background:  The role of IL-27 in the pathogenesis of airway inflammatory diseases remains elusive. We, therefore, have studied its concentrations in the sputum and plasma of patients with COPD and patients with pulmonary TB (PTB), and further investigated the mechanism-of-action effects of IL-27 on bronchial epithelial cells in vitro.

Methods:  Human bronchial epithelial cells grown on air-liquid interface culture were activated by IL-27, alone, or in combination with other inflammatory cytokines in the presence or absence of various signaling molecule inhibitors. The expression of CXCL10 was detected by reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay (ELISA). The underlying signaling pathways were studied by intracellular staining using flow cytometry, Western blot, ELISA, or siRNA.

Results:  Significantly higher sputum and plasma concentrations of IL-27 were found in patients with COPD (n = 34; P < .01 and P < .001, respectively) or patients with PTB (n = 31; P < .01 and P < .001, respectively) than in healthy control subjects (n = 48). Sputum, but not plasma, IL-27 levels in patients with COPD correlated negatively with FEV1 (r = −0.51, P < .01). Sputum, but not plasma, IL-27 in patients with PTB correlated positively with mycobacterial load in sputum (r = 0.48, P < .05). Further in vitro studies demonstrated that IL-27 could induce gene and protein expression of CXCL10 in bronchial epithelial cells, which was regulated by the activation of the phosphatidylinositol 3-OH kinase (PI3K)-Akt signaling pathway.

Conclusions:  The production of IL-27 is related to the pathogenesis of COPD and PTB, and IL-27 induces the expression of CXCL10 in bronchial epithelial cells through the activation of the PI3K-Akt signaling pathway.

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