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    Comparison of inflammatory cytokine release from nasal epithelial cells of non-atopic non-rhinitic, allergic rhinitic and polyp subjects and effects of diesel exhaust particles in vitro
    (Elsevier Doyma Sl, 2017) Ozturk, A. B.; Bayraktar, R.; Gogebakan, B.; Mumbuc, S.; Bayram, H.
    Background: Although studies have reported an association between air pollutants and increased allergic airway diseases, such as allergic rhinitis and nasal polyposis, the underlying mechanisms are not fully understood. A limited number of studies have suggested that diesel exhaust particles (DEP) play a role in atopy and the pathogenesis of allergic upper airway diseases. The aim of this study was to investigate the effect of DEP on inflammatory cytokine release, and mRNA expression of transcription factors such as JNK and NF-beta in primary nasal epithelial cells (NECs), in vitro. Methods: NECs from non-atopic, non-rhinitic subjects (controls) and patients with allergic rhinitis and nasal polyps were cultured and incubated with 0-100 mu g/nril DEP for 24 h. ELISA and RT-PCR were used to assess the release of IL-8, GM-CSF, and RANTES, and mRNA expression for JNK and NF-kappa B, respectively. Results: Compared to control cells, NECs from subjects with atopic polyps released significantly greater amounts of IL-8 (median = 887 vs. 176.6 pg/mu g cellular protein; p < 0.0001) and RANTES (median = 0.191 vs. 0.02 pg/mu g cellular protein; p < 0.001). While 50 mu g/ml DEP induced release of RANTES in NECs from patients with allergic rhinitis, 100 mu g/ml DEP decreased IL-8 levels in NECs from both control and allergic rhinitic subjects. DEP did not affect mRNA expression for JNK and NE-kappa B from NECs of subjects with polyps. Conclusions: NECs from subjects with various pathologies may respond differently to DEP. (C) 2017 SEICAR Published by Elsevier Espana, S.L.U. All rights reserved.
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    The role of bronchial epithelial cell apoptosis in the pathogenesis of COPD
    (Springer, 2014) Gogebakan, B.; Bayraktar, R.; Ulasli, M.; Oztuzcu, S.; Tasdemir, D.; Bayram, H.
    There is an increased airway inflammation in the pathogenesis of chronic obstructive pulmonary disease (COPD), and it has been suggested that there may also be problem in the apoptosis and renewal of cells. However, there are limited human airway cell studies, in particular those from larger airways such as bronchi. We cultured primary human bronchial epithelial cells (HBECs) from bronchial explants of smokers (n = 6) without COPD and smokers with COPD (n = 8). Apoptosis was studied by fluorescence activated cell sorting. qRT-PCR was used to assess mRNA expression for proteins involving apoptosis including p21(CIP1/WAF1), p53, caspase-8 and caspase-9. Although there was no difference in the rate of viable cells between cells from smokers and COPDs, the level of early apoptotic cells was significantly increased in COPD cells [mean +/- A standard error of mean (SEM) = 4.86 +/- A 3.2 %, p = 0.015] as compared to smokers (mean +/- A SEM = 2.71 +/- A 1.62 %). In contrast, the rate of late apoptotic cells was significantly decreased in COPD cells (mean +/- A SEM = 9.82 +/- A 5.71 %) comparing to smokers (mean +/- A SEM = 15.21 +/- A 5.08 %, p = 0.003). Although expression of mRNA for p21(CIP1/WAF1) and caspase-9 was similar in both groups, p53 and caspase-8 mRNA expression was significantly greater in COPD cells. These findings suggest that HBEC apoptosis is increased in COPD, and that this involves p53 and caspase-8 pathways.