Enhancement of Allergen-induced Eosinophilic Inflammation and Cytokine/Chemokine Expression Expression in the Murine Lungs by Asian Sand Dust

背景：亚洲沙尘（Kosa）中含有刺激性化学物质，如<2->SO^4.虽然Kosa会对呼吸系统健康产生不良影响，但没有实验研究显示Kosa对过敏性哮喘的影响。本研究旨在阐明Kosa对卵清蛋白（OVA）诱导的小鼠肺嗜酸性粒细胞炎症的影响。方法：ICR小鼠分别灌胃生理盐水、沙坡头沙（Kosa）、Kosa + SO_4<2->（Kosa-SO_4）、来自北京的天然亚洲尘（NAD）、OVA、OVA + Kosa、OVA + Kosa-SO_4或OVA + NAD。结果：三种沙尘均能加重哮喘大鼠气道嗜酸性粒细胞炎症反应，并伴有杯状细胞增殖，其中NAD作用最为明显。未观察到SO^_4的加和效应<2->。沙尘诱导的卵清蛋白（OVA）可抑制支气管肺泡灌洗液（BALF）中白细胞介素（IL）-1 2和干扰素（IFN）-γ的表达。与此相反，这些沙尘，特别是NAD，协同增加IL-5，嗜酸性粒细胞趋化因子，单核细胞趋化蛋白（MCP）-1在BALF和肺组织相关的OVA。NAD对IgG 1和IgE的产生具有佐剂效应。结论：这些结果表明，沙尘增强卵清蛋白诱导的嗜酸性粒细胞炎症在肺。假设这种增强是由IL-S与嗜酸性粒细胞趋化因子和MCP-1之间的协同作用通过抑制IL-12和IFN-γ诱导的。

Background: Asian sand dust (Kosa) contains irritant chemical species, such as SO^<2->_4. Although Kosa causes adverse respiratory health effects, there is no experimental study showing the effect of Kosa on allergic asthma. This study was undertaken to clarify the effects of Kosa on ovalbumin (OVA)-induced eosinophilic inflammation in the murine lung. Methods: ICR mice were administered intratracheally with saline; Kosa alone (sample from Shapotou desert); Kosa plus SO^<2->_4 (Kosa -SO_4); Natural Asian dust (NAD) from Beijing; OVA, OVA + Kosa; OVA + Kosa -SO_4; or OVA + NAD. Results: The three sand dusts, especially NAD, aggravated the eosinophilc airway inflammation accompanied by OVA-induced goblet cell proliferation. The additive effect of SO^<2->_4 was not observed. OVA which was induced by sand dusts suppressed the expression of interleukin (IL)-1 2 and interferon (IFN)-γ in bronchoalveolar lavage fluids (BALF). In contrast, these sand dusts, especially NAD, synergistically increased IL-5, eotaxin, and monocyte chemotactic protein (MCP)-1 in BALF and lung tissue related to OVA. NAD caused the adjuvant effects to IgG1 and IgE production. Conclusions: These results suggest that sand dusts enhance OVA-induced eosinophilic inflammation in the lungs. It is hypothesized that this enhancement is induced by the synergistic effect between IL-S and eotaxin and MCP-1 via the suppression of IL-12 and IFN-γ