Obstructive Lung Diseases: COPD II |

IL-17A Is Elevated in Patients With Chronic Obstructive Pulmonary Disease and Contributes to Airway Remodeling by Acting on Fibroblasts FREE TO VIEW

Tianwen Lai, PhD; Bao-ping Tian, PhD; Chao Zhang, PhD; Yue Hu, PhD; Luanqing Che, PhD; Feng Xu, PhD; Songmin Ying, PhD; Wen Li, PhD; Zhihua Chen, PhD; Huahao Shen, PhD
Author and Funding Information

Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, China

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;149(4_S):A379. doi:10.1016/j.chest.2016.02.394
Text Size: A A A
Published online


SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: Recent studies suggest that has been implicated in the pathogenesis of various inflammatory diseases. It is currently unknown, however, whether YKL-40 plays a role in COPD airway remodeling.

METHODS: Here, we evaluated IL-17A expression in the lung of patients with COPD and smokers without COPD, as well as in controls. The association between IL-17A expression and airway remodeling was analyzed. In parallel, IL-17A-/- mice and wild-type control animals were exposed to cigarette smoke for 3 months, and airway inflammation and airway remodeling were assessed. The effects of IL-17A on collagen synthesis of primary human lung fibroblasts were also evaluated.

RESULTS: Our data showed that IL-17A expression were elevated in the lung of COPD patients as compared to smokers without COPD and non-smokers. IL-17A expression correlated positively with collagen deposition. After exposing wild-type and IL-17A-/- mice to mainstream cigarette smoke (CS) for 3 months, IL-17A expression was increased in mice upon CS exposure. CS-treated IL-17A-/- mice exhibited reduced lung collagen content, smooth muscle area, mucus-producing cells, and inflammatory cell accumulation as compared with wild-type mice. Reduced matrix metalloproteinase-2 activity and expression of transforming growth factor-β1 and vascular endothelial growth factor were observed in CS-treated IL-17A-/- mice. Lung fibroblasts from IL-17A-/- mice showed reduced proliferation, migration, collagen deposition, and α-smooth muscle actin expression in comparison with CS-treated wild-type lung fibroblasts. Stimulation with IL-17A promoted collagen production in lung fibroblasts through ERK- and p38-dependent mechanisms.

CONCLUSIONS: we demonstrate that IL-17A is key for the development of CS-induced airway remodeling in COPD. In response to allergen, IL-17A induces the switching of lung fibroblasts to a pro-fibrogenic myofibroblast phenotype. The current data may provide insight into the underlying pathogenesis of COPD, in which IL-17A has an important pathogenic role.

CLINICAL IMPLICATIONS: IL-17A play an improtant in airway inflammation and airway remodeling. Thus, therapeutics targeting IL-17A might prove efficacious in the treatment of COPD.

DISCLOSURE: The following authors have nothing to disclose: Tianwen Lai, Bao-ping Tian, Chao Zhang, Yue Hu, Luanqing Che, Feng Xu, Songmin Ying, Wen Li, Zhihua Chen, Huahao Shen

No Product/Research Disclosure Information




Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

Find Similar Articles
CHEST Journal Articles
  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543