Background

Exposure to PM_2.5 has been associated with increased morbidity and mortality of lung diseases although the underlying mechanisms have not been fully uncovered. Airway inflammation is a critical event in the pathogenesis of lung diseases. This study aimed to examine the role of oxidative stress and epidermal growth factor receptor (EGFR) in PM_2.5-induced pro-inflammatory response in a human bronchial epithelial cell line, BEAS-2B.

Methods

BEAS-2B cells were exposed to 0, 20, 50, 100 and 150 μg/ml of PM_2.5. Secretion of pro-inflammatory mediators including interleukin-6 (IL-6), IL-8 and IL-1β was determined using enzyme linked immunosorbent assay. Levels of intracellular reactive oxygen species (ROS) were determined using flow cytometry. Phosphorylation of the EGFR was examined with immunoblotting.

Results

PM_2.5 exposure increased the secretion of IL-6, IL-8, and IL-1β in a concentration-dependent fashion. Moreover, exposure to PM_2.5 elevated intracellular levels of ROS, and phosphorylation of the EGFR (Y1068). Pretreatment of BEAS-2B cells with either an antioxidant or a specific EGFR inhibitor significantly reduced PM_2.5-induced IL-6, IL-8 and IL-1β secretion, implying that both oxidative stress and EGFR activation were involved in PM_2.5-induced pro-inflammatory response. Furthermore, pre-treatment of BEAS-2B cells with an antioxidant significantly blunted PM_2.5-induced EGFR activation, suggesting that oxidative stress was required for PM_2.5-induced EGFR activation.

Conclusion

PM_2.5 exposure induces pro-inflammatory response in human bronchial epithelial cells through oxidative stress-mediated EGFR activation.

中文翻译：

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氧化应激介导的表皮生长因子受体激活调节PM2.5诱导的人支气管上皮细胞促炎性介质的过度分泌。

背景

尽管尚未完全发现潜在的机制，但暴露于PM _2.5会增加肺部疾病的发病率和死亡率。气道炎症是肺部疾病发病机理中的关键事件。这项研究旨在检查氧化应激和表皮生长因子受体（EGFR）在人支气管上皮细胞系BEAS-2B中PM _2.5诱导的促炎反应中的作用。

方法

将BEAS-2B细胞暴露于0、20、50、100和150μg/ ml的PM _2.5中。使用酶联免疫吸附测定法测定包括白介素6（IL-6），IL-8和IL-1β在内的促炎性介质的分泌。使用流式细胞仪确定细胞内活性氧（ROS）的水平。用免疫印迹检查EGFR的磷酸化。

结果

PM _2.5暴露以浓度依赖的方式增加了IL-6，IL-8和IL-1β的分泌。此外，暴露于PM _2.5会升高细胞内ROS的水平，并使EGFR（Y1068）磷酸化。用抗氧化剂或特定的EGFR抑制剂预处理BEAS-2B细胞可显着降低PM _2.5诱导的IL-6，IL-8和IL-1β分泌，这暗示氧化应激和EGFR激活均与PM _2.5诱导的脯氨酸有关。 -炎症反应。此外，用抗氧化剂预处理BEAS-2B细胞可显着削弱PM _2.5诱导的EGFR激活，提示PM _2.5诱导的EGFR激活需要氧化应激。

结论

PM _2.5暴露通过氧化应激介导的EGFR激活诱导人支气管上皮细胞促炎反应。