NK T cell activation promotes Chlamydia trachomatis infection in vivo
NK T cell activation promotes Chlamydia trachomatis infection in vivo
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DOI：
10.4049/jimmunol.175.5.3197
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发表时间：
2005-09-01
影响因子：
4.4
通讯作者：
Yang, X
中科院分区：
文献类型：
--
作者：
Bilenki, L;Wang, SH;Yang, X
我们使用两种方法来研究NK T细胞（NKT）在细胞内细菌（沙眼衣原体小鼠肺炎（C muridarum））感染中的作用。一种是使用缺乏NKT的CD 1基因敲除（KO）小鼠，另一种是使用这些细胞的天然配体α-半乳糖神经酰胺（α-GalCer）激活NKT。数据显示NKT活化对衣原体肺部感染的促进作用。具体而言，与野生型小鼠相比，CD 1 KO小鼠表现出显著较低的体重减轻水平、较不严重的病理变化和较低的体内衣原体生长。免疫学分析显示，CD 1 KO小鼠的C.与野生型对照组相比，小鼠特异性IL-4和血清IgE Ab应答以及更明显的迟发型超敏反应。与KO小鼠中的发现一致，使用α-GalCer体内刺激NKT增强了体内衣原体生长，这与延迟型超敏反应减少和小鼠衣原体驱动的IL-4/IgE产生增加相关。此外，α-GalCer处理的BALB/c小鼠中IL-4活性的中和显著降低了α-GalCer处理对体内衣原体生长的促进作用。这些数据为NKT参与细菌发病机制及其在感染期间促进Th 2应答的作用提供了体内证据。
We used two approaches to examine the role of NK T cells (NKT) in an intracellular bacterial (Chlamydia trachomatis mouse pneumonitis (C muridarum)) infection. One is to use CD1 gene knockout (KO) mice, which lack NKT, and the other is to activate NKT using alpha-galactosylceramide (alpha-GalCer), a natural ligand of these cells. The data showed a promoting effect of NKT activation on Chlamydia lung infection. Specifically, CD1 KO mice exhibited significantly lower levels of body weight loss, less severe pathological change and lower chlarnydial in vivo growth than wild-type mice. Immunological analysis showed that CD1 KO mice exhibited significantly lower C. muridarum-specific IL-4 and serum IgE Ab responses as well as more pronounced delayed-type hypersensitivity response compared with wild-type controls. In line with the finding in KO mice, the in vivo stimulation of NKT using alpha-GalCer enhanced chlamydial growth in vivo, which were correlated with reduced delayed-type hypersensitivity response and increased C muridarum-driven IL-4/IgE production. Moreover, neutralization of IL-4 activity in the alpha-GalCer-treated BALB/c mice significantly reduced the promoting effect of alpha-GalCer treatment on chlarnydial growth in vivo. These data provide in vivo evidence for the involvement of NKT in a bacterial pathogenesis and its role in promoting Th2 responses during infection.