Abstract
BackgroundCigarettes smoking and IL-17A contribute to chronic obstructive pulmonary disease (COPD), and have synergistical effect on bronchial epithelial cell proliferation. CCAAT/enhancer-binding protein β (C-EBPβ) could be induced by IL-17A and is up-regulated in COPD. We explored the effect of cigarettes and IL-17 on bronchial epithelial–mesenchymal transition (EMT) in COPD mice and potential mechanism involved with C-EBPβ in this study.MethodsCOPD model was established with mice by exposing to cigarettes. E-Cadherin, Vimentin, IL-17A and C-EBPβ distributions were detected in lung tissues. Primary bronchial epithelial cells were separated from health mice and cocultured with cigarette smoke extract (CSE) or/and IL-17A. E-Cadherin, Vimentin and IL-17 receptor (IL-17R) expressions in vitro were assessed. When C-EBPβ were silenced by siRNA in cells, E-Cadherin, Vimentin and C-EBPβ expressions were detected.ResultsE-Cadherin distribution was less and Vimentin distribution was more in bronchus of COPD mice than controls. IL-17A and C-EBPβ expressions were higher in lung tissues of COPD mice than controls. In vitro, C-EBPβ protein expression was highest in CSE + IL-17A group, followed by CSE and IL-17A groups. E-cadherin expression in vitro was lowest and Vimentin expression was highest in CSE + IL-17A group, followed by CSE or IL-17A group. Those could be inhibited by C-EBPβ silenced.ConclusionsC-EBPβ mediates in cigarette/IL-17A-induced bronchial EMT in COPD mice. Our findings contribute to a better understanding on the progress from COPD to lung cancers, which will provide novel avenues in preventing tumorigenesis of airway in the context of cigarette smoking.
Highlights
Patients with chronic obstructive pulmonary disease (COPD) are shown an increase risk of lung cancer [1]
Cigarettes smoking induces airway epithelial– mesenchymal transition (EMT) of COPD mice Immunofluorescence staining showed that E-Cadherin distribution (Fig. 2a) was decreased and Vimentin distribution (Fig. 2c) was increased in bronchus of COPD group when compared with controls (Fig. 2b, d)
It’s even higher in cigarette smoke extract (CSE) + IL-17A group than CSE group or IL-17A group (Fig. 5). These results suggest that CSE or IL-17A could induce IL-17 receptor (IL-17R) expression in bronchial epithelial cells
Summary
Patients with COPD are shown an increase risk of lung cancer [1]. Epithelial–mesenchymal transition (EMT) in airway was found in COPD, which plays an important role in tumorigenesis [2, 3]. The obvious culprit linking COPD and lung cancer [4], could induce epithelial–mesenchymal transition (EMT) in airway [5]. Previous study found that CSE could enhance IL-17 receptor (IL17R) expression in human bronchial epithelial cell line 16HBE, and could synergistically work with IL-17A to induce proliferation of 16HBE [13]. Those findings indicate a synergistical effect of CSE and IL-17A on bronchial epithelial cell. We explored the effect of cigarettes and IL-17 on bronchial epithelial– mesenchymal transition (EMT) in COPD mice and potential mechanism involved with C-EBPβ in this study
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