医学
肿瘤坏死因子α
p38丝裂原活化蛋白激酶
趋化因子
呼吸道
成纤维细胞
信号转导
细胞因子
磷酸化
活力测定
污渍
信使核糖核酸
转录因子
免疫学
炎症
细胞生物学
呼吸系统
蛋白激酶A
内科学
生物
细胞
生物化学
基因
体外
作者
Dong Chang Lee,Hyunsu Choi,Jeong‐Min Oh,Yu-Pyo Hong,Su Hee Jeong,Choung‐Soo Kim,D.-G. Kim,Won‐Kyung Cho,Sung Won Kim,Soo Whan Kim,Jin Hee Cho,Joohyung Lee
摘要
Background Exposure to urban particulate matter (UPM) has been linked to aggravation of various health problems. Although the effects of UPM on the lower respiratory tract have been extensively studied, more research is required on the impact of UPM on the upper respiratory tract and the underlying mechanisms. Thus, we investigated the cytotoxic effects of UPM on cultured human nasal fibroblasts, the underlying signaling pathways involved, and changes in cytokine levels. Methods Human turbinate tissue specimens were collected during partial turbinectomies performed on 6 patients, and then cultured. The effect of UPM on nasal fibroblast viability was explored. Real‐time reverse transcription‐polymerase chain reaction was used to measure the mRNA levels of genes encoding cytokines and chemokines (interleukin [IL]‐4, IL‐6, IL‐8, and tumor necrosis factor‐α) before and after 24 hours of UPM treatment. Enzyme‐linked immunosorbent assays were employed to measure IL‐6 and IL‐8 levels. The status of the p38 and nuclear factor (NF)‐κB signaling pathways was analyzed by Western blotting. Results UPM reduced cell viability in a dose‐dependent manner and increased IL‐6 and IL‐8 expression at both the mRNA and protein levels. UPM induced the phosphorylation of p38 and NF‐κB p65; inhibitors of the actions of these proteins repressed phosphorylation and the expression of IL‐6 and IL‐8. Conclusion UPM induced IL‐6 and IL‐8 expression by fibroblasts via p38 and NF‐κB classical signaling, suggesting that UPM can induce or aggravate allergic and/or chronic rhinitis.
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