Allergy and Airway: Asthma IV |

Human β-defensin-2 and -3 Induce IL-8 Release Through CCR6 in Human Airway Smooth Muscle Cells FREE TO VIEW

Wei-Jia Wang; Xiao-Yan Qu; Xiao-Min Dang; Dong Shang; Dan Xu; Yong-Ping Shao; Wu-Yuan Lu; Ying Chang, PhD
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Center for Translational Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology and Frontier Institute of Science and Technology, Xi’an Jiaotong University, Xi'an, China

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

Chest. 2016;149(4_S):A41. doi:10.1016/j.chest.2016.02.043
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SESSION TYPE: Original Investigation Poster

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

PURPOSE: Human airway smooth muscle cells (HASMCs) play an important role in the pathogenesis of airway remodeling in asthma. HASMCs are involved in the inflammatory response through the release of inflammatory mediators. Human β-defensin (HBD) is a sub-family of small antimicrobial peptides, characterized by six conserved cysteines which compose a largely b-sheet structure by three intramolecular disulfides. Increasing evidence indicates that HBDs are related to pathogenesis of asthma. In this study, we investigated the effect of HBD-1, 2 and 3 on the release of pro-inflammatory cytokine IL-8 by HASMCs and explored the involving receptors.

METHODS: The HASMCs were simulated with 0μM, 1μM, 5μM and 10μM of HBD-1, 2 and 3 for 24h respectively. IL-8 level in cell supernatant was analyzed by ELISA, and cell viability was evaluated by WST-1 assay. In order to explore the involving receptor in HBDs-induced IL-8 production, the cells were pre-treated with the blocking antibody of CCR2, CCR6, TLR2 and TLR4.

RESULTS: HBD-2 and 3 but not HBD-1 significantly induced IL-8 production from HASMCs with a dose-dependent manner. However, 10μM of HBD-3 triggered significant cell death (Cell viability: 20.1±3.1% of control) although accompany with extremely higher IL-8 production (22.4±9.5 fold increase compared with control). The following results indicated that HBD-3-induced IL-8 production and cell death are independent. The administration of anti-oxidant reagent N-Acetylcysteine (NAC) could inhibit both IL-8 production and cell death induced by higher concentration of HBD-3. Furthermore, the blocking antibody against CCR6 could significantly inhibit IL-8 production induced by HBD-2 and 3.

CONCLUSIONS: HBD-2 and 3 could highly induce IL-8 production through CCR6 from HASMCs, and higher concentration of HBD3 independently triggered IL-8 release and cell death, which are due to oxidative stress in HASMCs.

CLINICAL IMPLICATIONS: HBD-2 and 3 may play important role in the pathogenesis of asthma by enhancing the release of pro-inflammatory cytokine IL-8 from HASMCs, which may open the new sight for target therapy of asthma.

DISCLOSURE: The following authors have nothing to disclose: Wei-Jia Wang, Xiao-Yan Qu, Xiao-Min Dang, Dong Shang, Dan Xu, Yong-Ping Shao, Wu-Yuan Lu, Ying Chang

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