Enhancement of antigen-induced eosinophilic inflammation in the airways of mast-cell deficient mice by diesel exhaust particles
Enhancement of antigen-induced eosinophilic inflammation in the airways of mast-cell deficient mice by diesel exhaust particles
复制标题
DOI：
10.1016/s0300-483x(02)00420-1
复制
发表时间：
2002-12-02
期刊：
影响因子：
4.5
通讯作者：
Shibamoto, T
中科院分区：
文献类型：
--
作者：
Ichinose, T;Takano, H;Shibamoto, T
本研究旨在阐明肥大细胞在柴油机尾气颗粒物（DEP）加重气道过敏性炎症和气道高反应性（AHR）中的作用。用肥大细胞缺陷小鼠（W/W ~ v）和正常小鼠（W/W ~+），通过嗜酸性粒细胞浸润、杯状细胞增殖和AHR，以及血浆中抗原特异性IgG 1和IgE的产生，检测了气道炎症。两组小鼠均经气管内注射卵清蛋白（OVA）或OVA+ DEP。在W/W+中，OVA促进的嗜酸性气道炎症和杯状细胞增殖显著大于W/W-v。在AHR中观察到类似的结果，但在两组小鼠中不显著。DEP增强了W/W-v中OVA诱导的过敏性气道炎症、杯状细胞增殖和AHR的发展，但在W/W+中没有。DEP降低了两组小鼠抗原特异性IgG 1和IgE的产生。肥大细胞在W/W-v中的主支气管粘膜下层中观察到。肥大细胞的数量被OVA处理显著减少。结果提示，肥大细胞在DEP引起W/W-v气道损伤和AHR的发生中不是必需的。然而，肥大细胞可能是OVA诱导的嗜嗜酸性炎症、杯状细胞增殖的气道损伤和W/W+的AHR所必需的。(C)2002年由Elsevier Science爱尔兰有限公司出版。
The present study was conducted to clarify the involvement of mast cells in the exacerbating effect of diesel exhaust particles (DEP) toward allergic airway inflammation and airway hyperresponsiveness (AHR). Airway inflammation by the infiltration of cosinophils with goblet cell proliferation and AHR, as well as by the production of antigen-specific IgG 1 and IgE, in plasma were examined using mast cell-deficient mice (W/W-v) and normal mice (W/W+). Both groups of mice received ovalbumin (OVA) or OVA+ DEP intratracheally. The eosinophilic airway inflammation and goblet cell proliferation promoted by OVA were significantly greater in W/W+ than in W/W-v. A similar result was observed in AHR, but was not significant among both groups of mice. DEP enhanced OVA induced-allergic airway inflammation, goblet cell proliferation, and development of AHR in W/W-v, but not in W/W+. DEP decreased production of antigen-specific IgG1 and IgE in both groups of mice. Mast cells were observed in the submucosal layer of the main bronchus in W/W-v. The number of mast cells was significantly decreased by OVA treatment. The results indicate that mast cells are not necessary to enhance airway damage and development of AHR in W/W-v by DEP. However, mast cells may be required for the OVA-induced cosinophilic inflammation, airway damage with goblet cell proliferation, and AHR in W/W+. (C) 2002 Published by Elsevier Science Ireland Ltd.