PDF(Pubmed)
Abstract：
Inflammatory bowel disease (IBD) is an immunologically complex disorder involving genetic, microbial, and environmental risk factors. Its global burden has continued to rise since industrialization, with epidemiological studies suggesting that ambient particulate matter (PM) in air pollution could be a contributing factor. Prior animal studies have shown that oral PM10 exposure promotes intestinal inflammation in a genetic IBD model and that PM2.5 inhalation exposure can increase intestinal levels of pro-inflammatory cytokines. PM10 and PM2.5 include ultrafine particles (UFP), which have an aerodynamic diameter of <0.10 μm and biophysical and biochemical properties that promote toxicity. UFP inhalation, however, has not been previously studied in the context of murine models of IBD. Here, we demonstrated that ambient PM is toxic to cultured Caco-2 intestinal epithelial cells and examined whether UFP inhalation affected acute colitis induced by dextran sodium sulfate and 2,4,6-trinitrobenzenesulfonic acid. C57BL/6J mice were exposed to filtered air (FA) or various types of ambient PM reaerosolized in the ultrafine size range at ~300 μg/m3, 6 h/day, 3-5 days/week, starting 7-10 days before disease induction. No differences in weight change, clinical disease activity, or histology were observed between the PM and FA-exposed groups. In conclusion, UFP inhalation exposure did not exacerbate intestinal inflammation in acute, chemically-induced colitis models.
摘要：
炎症性肠病（IBD）是一种涉及遗传，微生物，和环境风险因素。自工业化以来，它的全球负担持续上升，流行病学研究表明，空气污染中的环境颗粒物（PM）可能是一个促成因素。先前的动物研究表明，在遗传IBD模型中，口服PM10暴露会促进肠道炎症，而PM2.5吸入暴露会增加肠道促炎细胞因子的水平。PM10和PM2.5包括超细颗粒（UFP），其具有<0.10μm的空气动力学直径和促进毒性的生物物理和生化特性。UFP吸入,然而,以前没有在IBD的鼠模型中进行过研究。这里,我们证明了环境PM对培养的Caco-2肠上皮细胞具有毒性，并检查了UFP吸入是否会影响葡聚糖硫酸钠和2,4,6-三硝基苯磺酸诱导的急性结肠炎。将C57BL/6J小鼠暴露于过滤空气（FA）或各种类型的环境PM，在〜300μg/m3的超细尺寸范围内重新雾化，6小时/天，3-5天/周,疾病诱导前7-10天开始。体重变化没有差异，临床疾病活动，在PM和FA暴露组之间观察到组织学。总之,UFP吸入暴露不会加剧急性肠道炎症，化学诱导结肠炎模型。
