Song Jae-Jun, Lee Jong Dae, Lee Byung Don, Chae Sung Won, Park Moo Kyun
Department of Otolaryngology-Head and Neck Surgery, Dongguk University Ilsan Hospital, Ilsan, Republic of Korea.
Int J Pediatr Otorhinolaryngol. 2012 Mar;76(3):334-8. doi: 10.1016/j.ijporl.2011.12.003. Epub 2011 Dec 29.
In the present study, we investigate whether diesel exhaust particles (DEPs) cause cytotoxicity and induce inflammation or increase the expression of mucin in immortalized human middle ear epithelial cell lines (HMEECs). Several publications have shown an association between traffic-related air pollutants and otitis media. Additionally, DEP have been shown to cause inflammation and an allergic response in the airways.
Cell viability following DEP treatment was investigated in HMEECs using the MTT assay. We measured the expression of the inflammatory cytokines TNF-α and COX-2 and the mucin genes MUC5AC and MUC5B using semiquantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting.
Cell viability tests showed that exposure to more than 80 μg/mL of DEP caused a decrease in cell viability. DEP exposure also increased the expression of MUC5AC, but did not induce the expression of MUC5B in HMEECs.
DEP decreased cell viability, induced an inflammatory response, and increased mucin gene expression in HMEECs. These findings support the hypothesis that environmental diesel exposure is a risk factor for otitis media.
在本研究中，我们调查柴油尾气颗粒（DEP）是否会导致永生化人中耳上皮细胞系（HMEECs）产生细胞毒性、引发炎症或增加黏蛋白的表达。一些出版物表明，与交通相关的空气污染物与中耳炎之间存在关联。此外，已有研究表明DEP会导致气道炎症和过敏反应。
使用MTT法在HMEECs中研究DEP处理后的细胞活力。我们使用半定量实时逆转录-聚合酶链反应（RT-PCR）和蛋白质免疫印迹法测量炎性细胞因子TNF-α和COX-2以及黏蛋白基因MUC5AC和MUC5B的表达。
细胞活力测试表明，暴露于超过80μg/mL的DEP会导致细胞活力下降。DEP暴露还增加了HMEECs中MUC5AC的表达，但未诱导MUC5B的表达。
DEP降低了HMEECs的细胞活力，引发了炎症反应，并增加了黏蛋白基因的表达。这些发现支持了环境柴油暴露是中耳炎危险因素这一假设。
