中文摘要：

目的：观察肠道细菌代谢产物丁酸对体外培养小鼠骨髓源树突状细胞（Bone marrow derived dendritic cells，BMDCs）表型及功能的影响，并探讨其可能的机制。方法：利用丁酸盐对GM－CSF 和IL－4体外诱导的BMDCs 细胞进行处理，采用流式细胞术检测BMDCs 细胞表面分子CD80、CD86、MHCⅡ、B7－DC 的表达及其对T 细胞增殖的影响；用实时荧光定量PCR（RT－PCR）检测其细胞因子IL－6、IL－12的表达；用格里斯反应（Griess reaction）和免疫印迹法（Western blot）分别检测DC细胞产生NO2－的生成和Toll 样受体－4（TLR4）信号通路中ERK 分子的磷酸化。结果：丁酸可下调LPS 诱导的成熟BMDCs 细胞CD80、CD86、MHCⅡ、B7－DC 分子的表达。同时，丁酸也可抑制IL－6和IL－12的分泌，并抑制树突状细胞对OVA257－264抗原特异性T 细胞的增殖。进一步的Western blot 检测结果显示丁酸可抑制DC 细胞TLR4信号通路中ERK 分子的磷酸化。结论：丁酸可通过抑制DC 细胞TLR4信号通路中ERK 分子的磷酸化，下调DC 细胞的免疫功能。

英文摘要：

Objective：To investigate the effect of butyrate produced by bacterial metabolism on immune features of murine bone marrow-derived dendritic cells（BMDCs） and its potential mechanisms.Methods： BMDCs were prepared from bone marrow cells of C57BL/6 mice by being cultured with GM-CSF and IL-4.The expression of CD80,CD86,B7-DC and MHCⅡ on BMDCs and its pri-ming ability on the proliferation of OVA257-264 antigen specific CD8＋T cell were analyzed by using Flow cytometry.The mRNA levels of IL-6 and IL-12 in BMDCs were detected by real-time fluorescence quantitative PCR（q-PCR）.Simultaneously,Griess reaction and Western blot was used for analyzing the levels of NO2-in BMDCs culture supernatant and the ERK phosphortylation in BMDCs respectivly.Results：Butyrate could decrease the levels of CD80,CD86,MHCⅡand B7-DC,and downregulate the capability of BMDCs in priming the proliferation of CD8＋T cells.Furthermore,the secretions of IL-6,IL-12,NO2-and the phosphorylation of ERK were sup-pressed.Conclusion：Butyrate down-regulats the immune functions of BMDCs via inhibition of ERK phosphorylation in TLR 4 signaling pathway.