Diesel exhaust particles induced release of interleukin 6 and 8 by (primed) human bronchial epithelial cells (BEAS 2B) in vitro
Diesel exhaust particles induced release of interleukin 6 and 8 by (primed) human bronchial epithelial cells (BEAS 2B) in vitro
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DOI：
10.3109/01902149809046056
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发表时间：
1998-01-01
影响因子：
1.7
通讯作者：
Van Loveren, H
中科院分区：
文献类型：
--
作者：
Steerenberg, PA;Zonnenberg, JAJ;Van Loveren, H
最近的几项流行病学研究表明，过早死亡率的增加与环境颗粒空气污染有关。柴油机排气颗粒物（DEP）可能构成城市地区（超）细颗粒物空气污染的重要组成部分，因此可能有助于其毒性。呼吸道的上皮衬里可能是DEP毒性作用的第一靶点，暴露后可能释放促炎介质，如白细胞介素6和8（IL-6，IL-8），最终导致气道组织损伤和免疫改变。本研究观察了DEP（0.04-0.33 mg/mL）对人支气管上皮细胞株（BEAS-2B）产生IL-6、IL-8的影响。为了进行比较，还研究了暴露于二氧化硅和氧化钛（TiO 2）期间白细胞介素的产生，分别代表相对有毒和无毒的颗粒。扫描电镜和透射电镜观察表明，DEP颗粒的大小在25 ~ 35 nm之间，并能被BEAS-2B细胞吞噬。与未暴露的细胞相比，暴露于DEP 24或48 h后发现IL-6和IL-8产生增加（分别为11倍和4倍）。该增加低于二氧化硅（17倍和3.3倍），高于TiO 2，TiO 2未显示IL-6和IL-8增加。为了研究DEP对炎症致敏细胞的作用，将BEAS-2B细胞暴露于肿瘤坏死因子-α（TNF-α），随后暴露于DEP。暴露于TNF-α引起IL-6和IL-8产生的强烈增加。在TNF-α引发和随后暴露于DEP后，仅在低剂量的DEP和TNF-α（0.05-0.2 ng/mL）下，发现BEAS-2B细胞对IL-6和IL-8产生的累加效应。总之，BEAS-2B吞噬DEP并产生增加量的IL-6和IL-8。在TNF-alpha致敏的BEAS-2B细胞中，仅在低浓度的DEP和TNF-alpha下，DEP才增加白细胞介素的产生。这种促炎性白细胞介素的产生增加是否会影响免疫系统中的脆弱平衡，如T辅助细胞-1和T辅助细胞-2亚群的比例，从而导致对呼吸道感染的抵抗力改变或改变呼吸道过敏的表达，这是进一步研究的主题。
Several epidemiological studies have recently shown associations of increased premature mortality rates with ambient particulate air pollution. Diesel exhaust particles (DEP) may constitute an important part of (ultra)fine particulate air pollution in urban areas and may therefore contribute to its toxicity. Epithelial lining of the respiratory tract may be the first target of the toxic effects of DEP, that upon exposure may release pro-inflammatory mediators such as interleukin 6 and 8 (IL-6, IL-8), ultimately causing airway tissue damage and immune alterations. In this study the effects of in vitro DEP exposure (0.04-0.33 mg/mL) on IL-6, IL-8 production by a human bronchial epithelial cell line (BEAS-2B) were investigated. For comparison, the production of interleukins during exposure to silica and titanium oxide (TiO2) were also studied, representing relatively toxic and non-toxic particles, respectively. Scanning and transmission electron microscopy showed that the size of the DEP particles ranged between 25 to 35 nm and that DEP was phagocytized by BEAS-2B cells. An increase in IL-6 and IL-8 production (11- and 4-fold, respectively) was found after 24 or 48 h of exposure to DEP compared to the non-exposed cells. This increase was lower compared to silica (17- and 3.3-fold) and higher as compared to TiO2 which showed no increase for IL-6 and IL-8. To study the DEP effect on inflammation-primed cells, BEAS-2B cells were exposed to both tumor necrosis factor-alpha (TNF-alpha) and subsequently to DEP. Exposure to TNF-alpha caused a strong increase in IL-6 and IL-8 production. Additive effects on the IL-6 and IL-8 production by BEAS-2B cells were found after TNF-alpha priming and subsequently exposure to DEP, only at a low dose of DEP and TNF-alpha (0.05-0.2 ng/mL). In conclusion, BEAS-2B phagocytized DEP and produced an increased amount of IL-6 and IL-8. In TNF-alpha primed BEAS-2B cells, DEP increased interleukin production only at low concentrations of DEP and TNF-alpha. Whether this increased production of pro-inflammatory interleukins affects vulnerable balances in the immune system, such as T help-1 and T help-2 subsets ratios, resulting in an altered resistance to respiratory tract infections or altering the expression of respiratory allergy, is the subject of further studies.