Diesel exhaust particle-exposed human bronchial epithelial cells induce dendritic cell maturation and polarization via thymic stromal lymphopoietin

被引:97
作者
Bleck, Bertram [1 ]
Tse, Doris B. [1 ,2 ]
de Lafaille, Maria A. Curotto [3 ,4 ]
Zhang, Feijie [1 ]
Reibman, Joan [1 ,5 ]
机构
[1] NYU, Sch Med, Dept Med, Div Pulm & Crit Care Med, New York, NY 10011 USA
[2] NYU, Sch Med, Dept Med, Div Infect Dis, New York, NY USA
[3] NYU, Sch Med, Dept Pathol, Mol Pathogenesis Program, New York, NY USA
[4] NYU, Sch Med, Skirball Inst Biomol Med, New York, NY USA
[5] NYU, Sch Med, Dept Med & Environm Med, New York, NY USA
关键词
dendritic cells; bronchial epithelial cells; diesel exhaust particles; thymic stromal lymphopoietin; lung;
D O I
10.1007/s10875-007-9149-0
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Human exposure to air pollutants, including ambient particulate matter, has been proposed as a mechanism for the rise in allergic disorders. Diesel exhaust particles, a major component of ambient particulate matter, induce sensitization to neoallergens, but the mechanisms by which sensitization occur remain unclear. We show that diesel exhaust particles upregulate thymic stromal lymphopoietin in human bronchial epithelial cells in an oxidant-dependent manner. Thymic stromal lymphopoietin induced by diesel exhaust particles was associated with maturation of myeloid dendritic cells, which was blocked by anti-thymic stromal lymphopoietin antibodies or silencing epithelial cell-derived thymic stromal lymphopoietin. Dendritic cells exposed to diesel exhaust particle-treated human bronchial epithelial cells induced Th2 polarization in a thymic stromal lymphopoietin-dependent manner. These findings provide new insight into the mechanisms by which diesel exhaust particles modify human lung mucosal immunity.
引用
收藏
页码:147 / 156
页数:10
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