Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA 98195, USA.
Department of Medicine, University of Washington, Seattle, WA 98195, USA.
Toxicol Appl Pharmacol. 2019 Apr 1;368:55-62. doi: 10.1016/j.taap.2019.01.018. Epub 2019 Jan 23.
Quantum dot nanoparticles (QDs) are engineered nanomaterials (ENMs) that have utility in many industries due to unique optical properties not available in small molecules or bulk materials. QD-induced acute lung inflammation and toxicity in rodent models raise concerns about potential human health risks. Recent studies have also shown that some ENMs can exacerbate allergic airway disease (AAD). In this study, C57BL/6J and A/J mice were exposed to saline, house dust mite (HDM), or a combination of HDM and QDs on day 1 of the sensitization protocol. Mice were then challenged on days 8, 9 and 10 with HDM or saline only. Significant differences in cellular and molecular markers of AAD induced by both HDM and HDM + QD were observed between C57BL/6J and A/J mice. Among A/J mice, HDM + QD co-exposure, but not HDM exposure alone, significantly increased levels of bronchoalveolar lavage fluid (BALF). IL-33 compared to saline controls. BALF total protein levels in both mouse strains were also only significantly increased by HDM + QD co-exposure. In addition, A/J mice had significantly more lung type 2 innate lymphoid cells (ILC2s) cells than C57BL/6J mice. A/J lung ILC2s were inversely correlated with lung glutathione and MHC-II resident macrophages, and positively correlated with MHC-II resident macrophages. The results from this study suggest that 1) QDs influence HDM-induced AAD by potentiating and/or enhancing select cytokine production; 2) that genetic background modulates the impact of QDs on HDM sensitization; and 3) that potential ILC2 contributions to HDM induced AAD are also likely to be modulated by genetic background.
量子点纳米颗粒（QDs）是工程纳米材料（ENMs），由于其在小分子或体材料中不可用的独特光学特性，在许多行业中都有应用。QD 引起的啮齿动物模型中的急性肺炎症和毒性引起了对潜在人类健康风险的关注。最近的研究还表明，一些 ENMs 可以加重过敏性气道疾病（AAD）。在这项研究中，C57BL/6J 和 A/J 小鼠在致敏方案的第 1 天接受盐水、屋尘螨（HDM）或 HDM 和 QD 的组合暴露。然后，在第 8、9 和 10 天，用 HDM 或仅用盐水对小鼠进行攻毒。在 C57BL/6J 和 A/J 小鼠中，观察到由 HDM 和 HDM+QD 引起的 AAD 的细胞和分子标志物的显著差异。在 A/J 小鼠中，与单独暴露于 HDM 相比，HDM+QD 共暴露显著增加了支气管肺泡灌洗液（BALF）中的 IL-33 水平。与盐水对照相比。两种小鼠品系的 BALF 总蛋白水平也仅因 HDM+QD 共暴露而显著增加。此外，A/J 小鼠的肺 2 型固有淋巴细胞（ILC2）细胞明显多于 C57BL/6J 小鼠。A/J 肺 ILC2 与肺谷胱甘肽和 MHC-II 驻留巨噬细胞呈负相关，与 MHC-II 驻留巨噬细胞呈正相关。这项研究的结果表明：1）QD 通过增强和/或增强特定细胞因子的产生来影响 HDM 诱导的 AAD；2）遗传背景调节了 QD 对 HDM 致敏的影响；3）ILC2 对 HDM 诱导的 AAD 的潜在贡献也可能受到遗传背景的调节。
