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杜克雷嗜血杆菌与人类树突状细胞和巨噬细胞体外的相互作用
Interaction of Haemophilus Ducreyi with Human Monocyte-Derived Dendritic Cells and Macrophages in Vitro
【摘要】 为探讨抗原呈递细胞 (APCs)在软下疳发病机制中的作用 ,将树突状细胞 (DCs)和巨噬细胞 (MQs)与流感嗜血杆菌、杜克雷嗜血杆菌及其纯化抗原脂寡糖 (LOS)、细胞致死性肿胀毒素 (HdCDT)共育 ,测定它们的吞噬活性及6、2 4h时前炎症细胞因子TNF α、IL 1 β、IL 6、IL 8的分泌情况 ;将抗原作用后的细胞与自体CD4 + T淋巴细胞共育 ,测定T淋巴细胞增生及 48h细胞上清液中的细胞因子IFN γ、IL 4、IL 1 3的水平。结果 :约 6%~ 2 7%的DCs和 1 4%~ 2 6%的MQs吞噬杜克雷嗜血杆菌的不同菌株及无荚膜流感嗜血杆菌、大肠杆菌。杜克雷菌的不同菌株诱导DCs、MQs分泌大量的TNF α、IL 6、IL 8(P <0 .0 5 ) ;LOS诱导的前炎症细胞因子水平比细菌低 5 0 %~ 67% ;HdCDT不诱导任何前炎症细胞因子的产生。 2种细菌作用后的DCs、MQs能激活T淋巴细胞产生高水平IFN γ ,并诱导产生相似的T淋巴细胞增生 ,HdCDT无此作用。提示 :杜克雷菌能影响APCs活化T细胞的能力 ,并有助于Th1型反应。
【Abstract】 In order to elucidate the role of APCs in chancroid, the phagocytic activities and cytokine secretion profiles (TNF-α, IL-1α, IL-6 and IL-8) of the APCs were analyzed after 6 h, 24 h exposure to Haemophilus Influenzae, Haemophilus ducreyi bacteria and its purified antigens[H. ducreyi lipooligosaccharide (LOS) and cytolethal distending toxin (HdCDT)]. Furthermore, T-cell proliferation and cytokine (IFN-α, IL-4, IL-13) release were examined after co-culturing isolated autologous CD 4 + T-cells with antigen-pulsed APCs for 24 h. Results: Between 6% and 27% of the DCs, MQs phagocytosed different H. ducreyi strains, as wells as H. influenzae and E. coli. All of the H. ducreyi strains induced strong secretion of TNF-α, IL-6, IL-8(P<0.05); The purified LOS induced 2-to-3-fold lower levels of pro-inflammatory cytokines than whole bacteria, whereas HdCDT did not induce detectable levels of these cytokines. High levels of IFN-α and T-cell proliferation were induced by either DCs or MQs that were pre-exposed to H. ducreyi and H. influenzae bacteria. HdCDT-treated DCs and MQs did not induce T-cell proliferative responses and IFN-α secretion. Conclusions: H. ducreyi influences T-cell-stimulatory ability of APCs and favors a Th1-type response.
【Key words】 dendritic cells; macrophages; Haemophilus ducreyi; Haemophilus influenzae;
- 【文献出处】 首都医科大学学报 ,Journal of Capital University of Medical Sciences , 编辑部邮箱 ,2004年02期
- 【分类号】R378.4
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