Airborne Asian sand dust enhances murine lung eosinophilia
Airborne Asian sand dust enhances murine lung eosinophilia
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DOI：
10.3109/08958378.2010.510151
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发表时间：
2010-10-01
影响因子：
2.1
通讯作者：
Shibamoto, Takayuki
中科院分区：
文献类型：
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作者：
He, Miao;Ichinose, Takamichi;Shibamoto, Takayuki
没有实验研究证明空气中的亚洲沙尘（AASD）对过敏性肺嗜酸性粒细胞增多症的影响。在360 ℃下热处理30 min，排除从日本Iki岛大气中收集到的吸附到AASD上的有机物质。在小鼠肺中比较AASD或加热AASD（H-AASD）对过敏性肺炎的影响，以探讨有机物质的作用。ICR小鼠经气管内注射两种AASD和/或卵清蛋白（OVA）共4次，间隔2周。AASD和H-AASD增强了由OVA诱导的肺泡和气道粘膜下层中嗜酸性粒细胞的募集，其在支气管上皮中具有杯状细胞增殖。AASD和H-AASD协同增加全肺灌洗液中由OVA诱导的Th 2细胞因子-白细胞介素-13（IL-13）、嗜酸性粒细胞相关细胞因子和趋化因子（如IL-5）和单核细胞趋化蛋白-3（MCP-3）。AASD的增强作用明显大于H-AASD。AASD诱导佐剂对OVA特异性免疫球蛋白E（IgE）和IgG 1产生的影响。在使用RAW264.7细胞的体外研究中，AASD增加Toll样受体2（TLR 2）mRNA的表达，但不增加TLR 4 mRNA的表达。与对照组相比，AASD增加NALP 3、ASC和IL-1 β的mRNA表达。H-AASD没有引起任何mRNA的表达。这些结果表明，AASD中加重的肺嗜酸性粒细胞增多症是由于Th 2相关免疫应答的激活，并且微生物材料对TLR 2和NALP 3炎性体的激活可能参与了这种现象。
There is no experimental study demonstrating the effects of airborne Asian sand dust (AASD) on allergic lung eosinophilia. The organic substances adsorbed onto AASD collected from the atmosphere of Iki-island in Japan were excluded by heat treatment at 360 degrees C for 30 min. The effects of AASD or heated-AASD (H-AASD) towards allergic lung inflammation were compared in murine lungs to investigate the role of organic substances. ICR mice were administrated with the two kinds of AASD and/or ovalbumin (OVA) intratracheally four times at 2-week intervals. AASD and H-AASD enhanced eosinophil recruitment induced by OVA in the alveoli and in the submucosa of the airway, which has a goblet cell proliferation in the bronchial epithelium. AASD and H-AASD synergistically increased Th2 cytokines-interleukin-13 (IL-13), eosinophil-relevant cytokine and chemokine, such as IL-5, and monocyte chemotactic protein-3 (MCP-3) induced by OVA in whole lung lavage fluid. The enhancing effects were much greater in AASD than in H-AASD. AASD induced adjuvant effects on OVA-specific immunoglobulin E (IgE) and IgG1 production. In an in vitro study using RAW264.7 cells, AASD increased the expression of Toll-like receptors 2 (TLR2) mRNA, but not TLR4 mRNA. AASD increased mRNA expression of NALP3, ASC, and IL-1 beta compared with the control. H-AASD caused no expression of either mRNA. These results suggest that the aggravated lung eosinophilia in AASD is due to activation of a Th2-associated immune response and that the activation of TLR2 and NALP3 inflammasome by microbial materials could be participating in this phenomenon.