Braedel-Ruoff Sibylla, Faigle Marion, Hilf Norbert, Neumeister Birgid, Schild Hansjörg
Interfakultäres Institut für Zellbiologie der Universität Tübingen, Abteilung Immunologie, Tübingen, Germany.
J Endotoxin Res. 2005;11(2):89-96. doi: 10.1179/096805105X35189.
In this study, we analyzed the activation of bone-marrow derived dendritic cells (BMDCs) from mice lacking the cd14-gene with purified Legionella pneumophila lipopolysaccharide and with viable or formalin-killed L. pneumophila. We found that low concentrations of LPS and doses of L. pneumophila that are relevant to infection are dependent on CD14 to activate BMDCs. Higher concentrations of LPS are able to overcome the lack of CD14 indicating that other receptors areinvolved. We, therefore, included studies using BMDCs from mice lacking functional TLR2 and/or TLR4 molecules. We found that purified L. pneumophila LPS as well as L. pneumophila either viable or formalin-killed are able to activate BMDCs from TLR4-deficient C3H/HeJ mice but fail to activate BMDCs from TLR2-knockout mice. Our data show that not only purified LPS from L. pneumophila but also the microorganism itself stimulate BMDCs via TLR2 and that this stimulation is dependent on CD14 in this mouse model.
在本研究中,我们用纯化的嗜肺军团菌脂多糖以及活的或经福尔马林灭活的嗜肺军团菌,分析了缺乏cd14基因的小鼠骨髓来源树突状细胞(BMDCs)的激活情况。我们发现,与感染相关的低浓度脂多糖和嗜肺军团菌剂量激活BMDCs依赖于CD14。较高浓度的脂多糖能够克服CD14的缺失,这表明还有其他受体参与其中。因此,我们开展了使用缺乏功能性TLR2和/或TLR4分子的小鼠的BMDCs的研究。我们发现,纯化的嗜肺军团菌脂多糖以及活的或经福尔马林灭活的嗜肺军团菌均能够激活TLR4缺陷的C3H/HeJ小鼠的BMDCs,但无法激活TLR2基因敲除小鼠的BMDCs。我们的数据表明,不仅嗜肺军团菌的纯化脂多糖,而且微生物本身也通过TLR2刺激BMDCs,并且在该小鼠模型中这种刺激依赖于CD14。