Inflammatory and cytotoxic effects of acrolein, nicotine, acetylaldehyde and cigarette smoke extract on human nasal epithelial cells.
Inflammatory and cytotoxic effects of acrolein, nicotine, acetylaldehyde and cigarette smoke extract on human nasal epithelial cells.
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DOI：
10.1186/1471-2466-14-32
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发表时间：
2014-03-01
影响因子：
3.1
通讯作者：
Ennis M
中科院分区：
文献类型：
--
作者：
Comer DM;Elborn JS;Ennis M
香烟烟雾诱导气道上皮细胞的促炎反应，但目前尚不清楚香烟烟雾（CS）中所含的各种化学物质中的哪一种应被视为主要负责这些影响。我们假设，丙烯醛，尼古丁和乙醛，挥发性香烟烟雾中含有的重要化学物质，在诱导炎症和成瘾方面，在原代鼻上皮细胞培养物（PNEC）中具有免疫调节作用。来自19名健康受试者的PNEC在浸没培养物中生长，并在用铜绿假单胞菌脂多糖（PA LPS）刺激之前与丙烯醛、尼古丁或乙醛孵育。使用香烟烟雾提取物（CSE）重复实验以进行比较。ELISA法检测IL-8，ELISA法和Western blotting法检测NF-κB活性，Western blotting法检测caspase-3活性。采用Annexin-V染色和末端转移酶介导的dUTP缺口末端标记（TUNEL）法评价细胞凋亡。CSE在暴露24小时后是促炎性的，并且在该暴露时间后42%的细胞凋亡或坏死。丙烯醛对PNEC培养物具有促炎作用（30 μM暴露4 h诱导IL-8释放增加2.0倍），并且在PA LPS刺激后也增加IL-8释放。相比之下，尼古丁具有抗炎特性（50 μM尼古丁暴露24小时后，IL-8释放量为0.6倍），乙醛无作用。通过NF-κB活化测定，丙烯醛和尼古丁分别具有细胞刺激和抗炎作用。这两种化学物质都增加了切割的半胱天冬酶3的水平并诱导细胞死亡。在PNEC培养物中，丙烯醛是促炎性的，尼古丁是抗炎性的。CSE主要通过凋亡机制诱导细胞死亡。
Cigarette smoke induces a pro-inflammatory response in airway epithelial cells but it is not clear which of the various chemicals contained within cigarette smoke (CS) should be regarded as predominantly responsible for these effects. We hypothesised that acrolein, nicotine and acetylaldehyde, important chemicals contained within volatile cigarette smoke in terms of inducing inflammation and causing addiction, have immunomodulatory effects in primary nasal epithelial cell cultures (PNECs). PNECs from 19 healthy subjects were grown in submerged cultures and were incubated with acrolein, nicotine or acetylaldehyde prior to stimulation with Pseudomonas aeruginosa lipopolysaccharide (PA LPS). Experiments were repeated using cigarette smoke extract (CSE) for comparison. IL-8 was measured by ELISA, activation of NF-κB by ELISA and Western blotting, and caspase-3 activity by Western blotting. Apoptosis was evaluated using Annexin-V staining and the terminal transferase-mediated dUTP nick end-labeling (TUNEL) method. CSE was pro-inflammatory after a 24 h exposure and 42% of cells were apoptotic or necrotic after this exposure time. Acrolein was pro-inflammatory for the PNEC cultures (30 μM exposure for 4 h inducing a 2.0 fold increase in IL-8 release) and also increased IL-8 release after stimulation with PA LPS. In contrast, nicotine had anti-inflammatory properties (0.6 fold IL-8 release after 50 μM exposure to nicotine for 24 h), and acetylaldehyde was without effect. Acrolein and nicotine had cellular stimulatory and anti-inflammatory effects respectively, as determined by NF-κB activation. Both chemicals increased levels of cleaved caspase 3 and induced cell death. Acrolein is pro-inflammatory and nicotine anti-inflammatory in PNEC cultures. CSE induces cell death predominantly by apoptotic mechanisms.
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单一与反复的香烟烟雾暴露后，支气管趋化因子表达不同。
影响因子：
5.8
作者：
Betsuyaku, Tomoko;Hamamura, Ichiro;Hata, Junko;Takahashi, Hiroshi;Mitsuhashi, Hiroaki;Adair-Kirk, Tracy L.;Senior, Robert M.;Nishimura, Masaharu
通讯作者：
Nishimura, Masaharu
影响因子：
5.8
作者：
Demedts, Ingel K.;Demoor, Tine;Bracke, Ken R.;Joos, Guy F.;Brusselle, Guy G.
通讯作者：
Brusselle, Guy G.
影响因子：
3.7
作者：
Comer, David M.;Elborn, J. Stuart;Ennis, Madeleine
通讯作者：
Ennis, Madeleine
DOI：
10.1165/rcmb.2008-0131oc
发表时间：
2009-08-01
影响因子：
6.4
作者：
Groskreutz, Dayna J.;Monick, Martha M.;Hunninghake, Gary W.
通讯作者：
Hunninghake, Gary W.
影响因子：
4.3
作者：
Hurst, JR;Wilkinson, TMA;Wedzicha, JA
通讯作者：
Wedzicha, JA