Background

Exposure to particulate matter (PM) air pollution is associated with adverse health outcomes in children with cystic fibrosis (CF). Airway macrophages (AM) phagocytose and retain inhaled PM in vivo, and the area of carbon in AM reflects both inhaled PM dose and phagocytic function. Since airway prostaglandin-E₂ (PGE₂) is increased in CF, and PGE₂ suppresses AM phagocytosis, we sought evidence for PGE₂-mediated suppression of AM phagocytosis of inhaled carbonaceous PM in CF.

Methods

After informed consent, urine was obtained from 20 controls and 24 CF children. In the subgroup of older children, at least one induced sputum was done in 20 controls and 19 CF children. Urinary tetranor PGEM, the major metabolite of PGE₂, and sputum PGE₂ were measured by mass spectrometry. The area of carbon in AM was determined by image analysis. Exposure to PM was assessed by modelling and personal monitoring. The effect of either PGE₂ or CF sputum supernatant on phagocytosis of diesel exhaust particle (DEP) by AM was assessed in vitro. Data were analysed by t-test.

Results

Both urinary tetranor PGEM (P<0.05), and sputum PGE₂ (P<0.05) were increased in CF . Despite no difference in PM exposure between groups, the area of phagocytosed carbon by AM was decreased in children with CF (P<0.01). PGE₂ suppressed phagocytosis of DEP by AM from both controls and CF (P<0.0001). CF sputum supernatant suppressed phagocytosis of DEP by AM (P<0.0001) in a PGE₂-dependent manner.

Conclusion

Increased PGE₂ in the CF airway suppresses phagocytosis of inhaled PM by AM.

中文翻译：

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前列腺素 E2 和气道巨噬细胞对囊性纤维化吸入颗粒物的吞噬作用

背景

暴露于颗粒物 (PM) 空气污染与囊性纤维化 (CF) 儿童的不良健康结果相关。气道巨噬细胞 (AM)在体内吞噬并保留吸入的 PM ，AM 中的碳面积反映了吸入的 PM 剂量和吞噬功能。由于气道前列腺素-E ₂ (PGE ₂ ) 在 CF 中增加，并且 PGE ₂抑制 AM 吞噬作用，我们寻找 PGE ₂介导的对 CF 中吸入碳质 PM 的 AM 吞噬作用的抑制的证据。

方法

在知情同意后，从 20 名对照和 24 名 CF 儿童中获得尿液。在年龄较大的儿童亚组中，20 名对照组和 19 名 CF 儿童至少进行了一次诱导痰。_{PGE 2}的主要代谢物尿四甲基PGEM和痰PGE ₂用质谱法测定。AM中碳的面积是通过图像分析确定的。通过建模和个人监测评估对 PM 的暴露。在体外评估了PGE ₂或 CF 痰上清液对 AM 对柴油机尾气颗粒 (DEP) 的吞噬作用。通过t检验分析数据。

结果

CF组尿四氢呋喃PGEM（P <0.05）和痰PGE ₂（P <0.05）均升高。尽管组间 PM 暴露无差异，但 CF 患儿 AM 吞噬碳的面积减少（P <0.01）。PGE ₂抑制来自对照组和 CF 的 AM 对 DEP 的吞噬作用（P <0.0001）。CF 痰上清液以 PGE ₂依赖性方式抑制 AM 对 DEP 的吞噬作用 ( P <0.0001)。

结论

CF 气道中增加的 PGE ₂抑制了 AM 对吸入 PM 的吞噬作用。