Diesel exhaust particles enhance antigen-induced airway inflammation and local cytokine expression in mice
Diesel exhaust particles enhance antigen-induced airway inflammation and local cytokine expression in mice
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DOI：
10.1164/ajrccm.156.1.9610054
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发表时间：
1997-07-01
影响因子：
24.7
通讯作者：
Sagai, M
中科院分区：
文献类型：
--
作者：
Takano, H;Yoshikawa, T;Sagai, M
以往的实验研究表明，鼻腔滴注柴油机尾气颗粒物(DEP)可以增强鼻腔免疫球蛋白E应答和细胞因子的产生。然而，没有实验证据表明DEP与过敏性哮喘有关。我们研究了气管内接种DEP对抗原诱导的小鼠气道炎症、细胞因子蛋白的局部表达和抗原特异性免疫球蛋白产生的影响。DEP加重了以嗜酸性粒细胞和淋巴细胞的浸润为特征的卵蛋白诱导的气道炎症，并增加了支气管上皮中的杯状细胞。DEP与抗原或DEP相比，肺组织和支气管肺泡灌洗液中IL-5蛋白水平明显升高。只有副警长一人。DEP与抗原联合作用后，局部IL-4、粒细胞巨噬细胞集落刺激因子(GM-CSF)和IL-2的表达显著增加，而干扰素-γ的表达不受影响，且DEP对抗原特异性的免疫球蛋白和IgE的产生具有佐剂作用。这些结果首次为DEP增强过敏性哮喘的表现提供了实验证据。这种增强可能主要是通过局部IL-5表达的增加以及IL-4、GM-CSF和IL-2的调节表达来实现的。
Previous experimental studies have suggested that nasal instillation of diesel exhaust particles (DEP) can enhance nasal IgE response and cytokine production. However, there is no experimental evidence for the relation of DEP to allergic asthma. We investigated the effects of DEP inoculated intra tratracheally on antigen-induced airway inflammation, local expression of cytokine proteins, and antigen-specific immunoglobulin production in mice, DEP aggravated ovalbumin-induced airway inflammation characterized by infiltration of eosinophils and lymphocytes and an increase in goblet cells in bronchial epithelium. DEP with antigen markedly increased interleukin-5 (IL-5) protein levers in lung tissue and bronchoalveolar ravage supernatants compared with either antigen or. DEP alone. The combination of DEP and antigen induced significant increases in local expression of IL-4, granulocyte macrophage-colony stimulating Factor (GM-CSF), and IL-2 whereas expression of interferon-gamma war not affected, In addition, DEP exhibited adjuvant activity for the antigen-specific production of IgG and IgE, These results provide the first experimental evidence that DEP can enhance the manifestations of allergic asthma. The enhancement may be mediated mainly by the increased local expression of IL-5, and also by the modulated expression of IL-4 GM-CSF, and IL-2.