Ultrafine but not fine particulate matter causes airway inflammation and allergic airway sensitization to co-administered antigen in mice
Ultrafine but not fine particulate matter causes airway inflammation and allergic airway sensitization to co-administered antigen in mice
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DOI：
10.1111/j.1365-2222.2006.02586.x
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发表时间：
2006-11-01
影响因子：
6.1
通讯作者：
Pieters, R.
中科院分区：
文献类型：
--
作者：
de Haar, C.;Hassing, I.;Pieters, R.
背景空气中的颗粒物（PM）是与呼吸道过敏发病率增加相关的重要因素。PM对过敏性致敏的佐剂作用是其可能的作用机制之一，而气道炎症的诱导在PM诱导的佐剂作用中起重要作用。目的由于不同粒径的PM具有不同的毒性潜能，我们研究了粒径在PM诱导气道炎症和过敏性致敏中的作用。这是使用细（0.250和0.260 μ m）和超细（0.029和0.014 μ m）二氧化钛（TiO 2）和炭黑颗粒（CBP）与已知的差异，在气道toxicity.Methods小鼠鼻内暴露于卵清蛋白（OVA）单独或结合不同的颗粒之一。在第8天，在肺和肺引流支气管周围淋巴结（PBLN）中研究气道炎症的诱导和免疫佐剂活性。在第21天测量OVA特异性抗体，并在OVA激发后（第28天）研究过敏性气道炎症的发展。结果当给予相同的总颗粒质量（200 μ g）时，暴露于超细TiO 2和CBP诱导的气道炎症，并具有免疫佐剂活性。后者通过增加PBLN细胞数量和OVA特异性辅助性T细胞2型（Th 2）细胞因子（IL-4、IL-5、IL-10和IL-13）的产生来显示。然而，血清中的OVA特异性IgE和IgG 1水平仅在暴露于超细TiO 2的动物中增加，在用OVA激发后，在超细TiO 2和CBP处理组中均可以检测到过敏性气道炎症。引起气道炎症，并在当前模型中具有免疫佐剂活性，支持颗粒毒性是位点依赖性的并与佐剂活性相关的假设。
Background Airborne particulate matter (PM) is an important factor associated with the enhanced prevalence of respiratory allergy. The PM adjuvant activity on allergic sensitization is a possible mechanism of action involved, and the induction of airway inflammation is suggested to be of importance in PM-induced adjuvant activity.Objective Because differently sized PM have different toxic potentials, we studied the role of particle size in the induction of airway inflammation and allergic sensitization. This was done using fine (0.250 and 0.260 mu m) and ultrafine (0.029 and 0.014 mu m) titanium dioxide (TiO2) and carbon black particles (CBP) with known differences in airway toxicity.Methods Mice were intranasally exposed to ovalbumin (OVA) alone or in combination with one of the different particles. The induction of airway inflammation and the immune adjuvant activity were studied in the lungs and lung-draining peribronchial lymph nodes (PBLN) at day 8. OVA-specific antibodies were measured at day 21, and the development of allergic airway inflammation was studied after OVA challenges (day 28).Results When administered at the same total particle mass (200 mu g), exposure to ultrafine TiO2 and CBP-induced airway inflammation, and had immune adjuvant activity. The latter was shown by increasing both the PBLN cell numbers and the production of OVA-specific T-helper type 2 (Th2) cytokines (IL-4, IL-5, IL-10 and IL-13). Whereas OVA-specific IgE and IgG1 levels in serum were only increased in animals exposed to the ultrafine TiO2, allergic airway inflammation could be detected in both ultrafine TiO2- and CBP-treated groups after challenges with OVA.Conclusion Our data show that only the ultrafine particles, with a small diameter and a large total surface area/mass, cause airway inflammation and have immune adjuvant activity in the current model supporting the hypothesis that particle toxicity is site-dependent and related to adjuvant activity.