The effects of microbial materials adhered to Asian sand dust on allergic lung inflammation
The effects of microbial materials adhered to Asian sand dust on allergic lung inflammation
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DOI：
10.1007/s00244-007-9128-8
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发表时间：
2008-10-01
影响因子：
4
通讯作者：
Shibamoto, T.
中科院分区：
文献类型：
--
作者：
Ichinose, T.;Yoshida, S.;Shibamoto, T.
据报道，亚洲沙尘（ASD）含有来自中国东部空气污染物的微生物物质、硫酸盐（SO 42）和硝酸盐（NO3-），会对呼吸系统健康造成不良影响。ASD使卵清蛋白（OVA）相关的实验性肺嗜酸性粒细胞增多症加重。本研究采用360 ℃热处理30 min的方法，将吸附在ASD上的有毒物质排出体外，比较了未加热ASD和加热ASD（H-ASD）对小鼠肺变应性炎症的影响。ICR小鼠经气管内给予生理盐水（对照）、H-ASD、ASD、OVA、OVA + H-ASD和OVA + ASD，间隔2周，共4次。ASD仅增加支气管肺泡灌洗液（BALF）中的中性粒细胞沿着促炎介质，如角质形成细胞趋化因子（KC）。H-ASD和ASD增强了肺泡和气道粘膜下层中由OVA诱导的嗜酸性粒细胞募集，其在支气管上皮中具有杯状细胞增殖。两种ASD协同增加BALF中与OVA相关的白细胞介素-5（IL-5）、单核细胞趋化蛋白-3（MCP-3）和嗜酸性粒细胞趋化因子。ASD的增强作用明显大于H-ASD。两种ASD均能诱导卵清蛋白产生特异性IgE和IgG 1。在体外实验中，ASD可增加RAW 264.7细胞Toll样受体2（TLR 2）mRNA的表达，但对TLR 4 mRNA的表达无影响。H-ASD不引起TLR mRNA的表达。这些结果表明，ASD导致的肺部嗜酸性粒细胞增多症加重可能是由于粘附在ASD上的微生物成分激活TLR 2而激活Th 2相关免疫反应所致。
Asian sand dust (ASD) containing microbiological materials, sulfate (SO42 ), and nitrate (NO3-) derived from air pollutants in East China, reportedly cause adverse respiratory health effects. ASD aggravates ovalbumin (OVA)-associated experimental lung eosinophilia. In this study, the toxic materials adsorbed onto ASD were excluded by heat treatment at 360C for 30 min. The effects of nonheated ASD or heated ASD (H-ASD) toward the allergic lung inflammation were compared in murine lungs. ICR mice were administered intratracheally with normal saline (control), H-ASD, ASD, OVA, OVA + H-ASD, and OVA + ASD, four times at 2-week intervals. ASD only increased neutrophils in bronchoalveolar lavage fluids (BALFs) along with pro-inflammatory mediators, such as keratinocyte chemoattractant (KC). H-ASD and ASD 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. The two ASDs synergistically increased interleukin-5 (IL-5), monocyte chemotactic protein-3 (MCP-3), and eotaxin, which were associated with OVA, in BALF. The enhancing effects were much greater in ASD than in H-ASD. The two ASDs induced the adjuvant effects to specific IgE and IgG1 production by OVA. In the in vitro study using RAW264.7 cells, ASD increased the expression of Toll-like receptor 2 (TLR 2) mRNA but not TLR4 mRNA. H-ASD caused no expression of either TLR mRNA. These results suggest that the aggravated lung eosinophilia by ASD may be due to activation of Th2-associated immune response via the activation of TLR2 by microbial components adhered to ASD.