کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2541129 1122642 2010 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Inactivation of IκB-kinase-β dependent genes in airway epithelium reduces tobacco smoke induced acute airway inflammation
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
پیش نمایش صفحه اول مقاله
Inactivation of IκB-kinase-β dependent genes in airway epithelium reduces tobacco smoke induced acute airway inflammation
چکیده انگلیسی

We have examined the role of NF-κB regulated genes in airway epithelium in mediating tobacco smoke induced airway inflammation in studies of CC10-Cretg/IkkβΔ/Δ mice in which NF-κB signaling through IκB-kinase-β (IKK-β) is selectively ablated in epithelial cells in the airway. CC10-Cretg/IkkβΔ/Δ mice exposed to tobacco smoke for seven days had a significant decrease in the number of BAL cells (total cells, neutrophils, and macrophages) as well as significantly reduced numbers of peribronchial cells (F4/80+ and myeloperoxidase+) compared to tobacco exposed WT mice. In addition to the reduction in peribronchial cells, CC10-Cretg/IkkβΔ/Δ mice exposed to tobacco smoke had a significant decrease in the number of macrophages and neutrophils in the alveolar space suggesting that inactivation of NF-κB in the airway epithelium influenced the number of neutrophils and macrophages recruited to the alveolus. Levels of the NF-κB regulated chemokines KC and MCP-1 were significantly reduced in lungs of tobacco smoke exposed CC10-Cretg/IkkβΔ/Δ mice compared to tobacco exposed WT mice. In contrast, there was no significant difference in levels of NF-κB regulated MIP-1α between CC10-Cretg/IkkβΔ/Δ and WT mice. Lung sections of tobacco smoke exposed CC10-Cretg/IkkβΔ/Δ mice immunostained with KC or MCP-1 antibodies demonstrated reduced expression of these chemokines in the airway epithelium, but not in alveolar epithelium. Overall, these studies demonstrate an important role for NF-κB regulated genes in airway epithelium in contributing to acute tobacco smoke induced airway inflammation not only in the peribronchial space but also in the alveolar space.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: International Immunopharmacology - Volume 10, Issue 8, August 2010, Pages 906–912
نویسندگان
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