scholarly journals The Protective Effect of HBO1 on Cigarette Smoke Extract-Induced Apoptosis in Airway Epithelial Cells

2020 ◽  
Vol Volume 15 ◽  
pp. 15-24
Author(s):  
Lin Chen ◽  
Lijuan Luo ◽  
Naixin Kang ◽  
Xue He ◽  
Tiao Li ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Protective Effect ◽  
Cigarette Smoke ◽  
Cigarette Smoke Extract ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Induced Apoptosis

scholarly journals A Protective Role of FAM13A in Human Airway Epithelial Cells Upon Exposure to Cigarette Smoke Extract

2021 ◽  
Vol 12 ◽  
Author(s):  
Qing Chen ◽  
Maaike de Vries ◽  
Kingsley Okechukwu Nwozor ◽  
Jacobien A. Noordhoek ◽  
Corry-Anke Brandsma ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoking ◽  
Cigarette Smoke ◽  
Airway Epithelium ◽  
Barrier Function ◽  
Cigarette Smoke Extract ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Copd Patients ◽  
Epithelial Resistance

BackgroundChronic Obstructive Pulmonary Disease (COPD) is a progressive lung disease characterized by chronic inflammation upon inhalation of noxious particles, e.g., cigarette smoke. FAM13A is one of the genes often found to be associated with COPD, however its function in the pathophysiology of COPD is incompletely understood. We studied its role in airway epithelial barrier integrity and cigarette smoke-induced epithelial responses.Materials and MethodsProtein level and localization of FAM13A was assessed with immunohistochemistry in lung tissue from COPD patients and non-COPD controls. In vitro, FAM13A expression was determined in the absence or presence of cigarette smoke extract (CSE) in primary airway epithelial cells (AECs) from COPD patients and controls by western blotting. FAM13A was overexpressed in cell line 16HBE14o- and its effect on barrier function was monitored real-time by electrical resistance. Expression of junctional protein E-cadherin and β-catenin was assessed by western blotting. The secretion of neutrophil attractant CXCL8 upon CSE exposure was measured by ELISA.ResultsFAM13A was strongly expressed in airway epithelium, but significantly weaker in airways of COPD patients compared to non-COPD controls. In COPD-derived AECs, but not those of controls, FAM13A was significantly downregulated by CSE. 16HBE14o- cells overexpressing FAM13A built up epithelial resistance significantly more rapidly, which was accompanied by higher E-cadherin expression and reduced CSE-induced CXCL8 levels.ConclusionOur data indicate that the expression of FAM13A is lower in airway epithelium of COPD patients compared to non-COPD controls. In addition, cigarette smoking selectively downregulates airway epithelial expression of FAM13A in COPD patients. This may have important consequences for the pathophysiology of COPD, as the more rapid build-up of epithelial resistance upon FAM13A overexpression suggests improved (re)constitution of barrier function. The reduced epithelial secretion of CXCL8 upon CSE-induced damage suggests that lower FAM13A expression upon cigarette smoking may facilitate epithelial-driven neutrophilia.

scholarly journals Cigarette smoke extract modulates respiratory defence mechanisms through effects on T-cells and airway epithelial cells

2006 ◽  
Vol 100 (5) ◽  
pp. 818-827 ◽  
Author(s):  
Pernilla Glader ◽  
Sebastian Möller ◽  
Johanna Lilja ◽  
Elisabet Wieslander ◽  
Claes-Göran Löfdahl ◽  
...  
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Cigarette Smoke Extract ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Defence Mechanisms
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