Epidemiologic studies have reported the association between fine particles (aerodynamic diameter ≤ 2.5 μm; PM2.5) and health effects, but the immunological mechanisms are not clear. To investigate the dose and time-dependent role of toll-like receptor (TLR) and Th1/Th2 shift in local and systemic inflammation induced by PM2.5, mice were subjected to intratracheal instillation of 2.5, 5, or 10 mg/kg PM2.5 in this study. After 24 h, 72 h, 7 days, and 14 days, mice were sacrificed to measure TLR2 and TLR4 expressions and Th1/Th2 related cytokines in bronchoalveolar lavage fluid (BALF) and peripheral blood. Histopathological changes in lung were also examined. Inflammatory infiltration and macrophages with engulfed particles were found by lung histopathology after PM2.5 exposure. TLR4 positive cells decreased in BALF but increased in blood at 24 h after the exposure. The low percentage of TLR4 positive cells continued to day 14 in BALF, but recovered at day 7 and decreased further to lower than the control value at day 14 in blood. TLR2 positive cell changed similar to TLR4 in BALF on the dose effects. In BALF at 24 h after the exposure, the Th2 related cytokines IL-5 and IL-10 increased dose-dependently; and in blood, the Th2 related cytokines IL-4, IL-5, and IL-10 also increased. These results suggest that acute exposure of PM2.5 leads to acute inflammatory responses locally and systemically in mice. TLR2 and TLR4 are involved in this process and PM2.5 can drive a Th2-biased immune response.

译文

:流行病学研究已经报告了微粒(空气动力学直径≤2.5μm; PM2.5)与健康影响之间的关联,但免疫机制尚不清楚。为了研究Toll样受体(TLR)和Th1 / Th2转移在PM2.5诱导的局部和全身炎症中的剂量和时间依赖性作用,对小鼠进行气管内滴注2.5、5或10μmg/ kg PM2 .5在这项研究中。在24小时,72小时,7天和14天后,处死小鼠以测量支气管肺泡灌洗液(BALF)和外周血中TLR2和TLR4的表达以及Th1 / Th2相关的细胞因子。还检查了肺的组织病理学变化。 PM2.5暴露后通过肺组织病理学发现炎症浸润和吞噬颗粒的巨噬细胞。暴露24h后,BALF中TLR4阳性细胞减少,但血液中TLR4阳性细胞增加。在BALF中,TLR4阳性细胞的低百分比持续至第14天,但在第7天恢复,并且在血液中第14天进一步下降至低于对照值。在剂量效应上,TLR2阳性细胞的变化与BALF中的TLR4相似。暴露后24h,在BALF中,与Th2相关的细胞因子IL-5和IL-10呈剂量依赖性增加。在血液中,与Th2相关的细胞因子IL-4,IL-5和IL-10也增加。这些结果表明,PM2.5的急性暴露导致小鼠局部和全身急性炎症反应。 TLR2和TLR4参与了这一过程,而PM2.5可以驱动偏向Th2的免疫反应。

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