丁酸钠及其G蛋白偶联受体对T淋巴细胞的调节作用  

Regulation effect of butyrate and its GPCR receptor on T lymphocytes

作　　者：马钰[1] 刘兰德[1] 刘方[1] 韩姬[1] 刘明耀[1] 陈华青[1] 

机构地区：[1]上海市调控生物学重点实验室,华东师范大学生命科学学院生命医学研究所,上海200241

出　　处：《现代免疫学》2012年第6期501-505,共5页Current Immunology

基　　金：上海市科学技术委员会重点实验室建设(11DZ2260300)

摘　　要：短链脂肪酸通常由肠道微生物对食物纤维的发酵而产生,已有报道其在免疫和炎症中起重要作用。本文研究丁酸钠通过其受体GPR43对T淋巴细胞的调节作用,探讨丁酸钠在T细胞水平的抗炎作用和机制。以Hut78和Jurkat细胞株为模型,用RT-PCR检测T细胞中GPR41和GPR43的表达情况。用实时荧光定量PCR检测PMA/Ionomycin诱导的T淋巴细胞经丁酸钠处理后IL-2和IL-4水平变化,并以ELISA等方法验证。通过RT-PCR以及胞内钙离子检测探究丁酸钠对T细胞的具体作用机制及作用靶标。结果显示,GPR41和GPR43在T细胞中存在表达且在PMA刺激后表达显著上升。丁酸钠能刺激胞内钙离子的释放,抑制IL-2、促进IL-4的产生,且这种调节作用不受Gαi抑制剂PTX影响。另外,丁酸钠可以显著抑制MOG诱导EAE小鼠脾脏淋巴细胞的体外增殖。这些结果说明,在T淋巴细胞中丁酸钠主要通过GPR43受体调节其细胞因子的产生,抑制炎症性T淋巴细胞的增殖从而发挥其抗炎功能。The short chain fatty acids,which are produced by fermentation of dietary fibre by intestinal microbiota, have impli-cations in immune responses and inflammation. The present study reports the effect of butyrate and its GPCR receptor on T lymphocytes, and the anti-inflammatory mechanism was analyzed. GPR41 and GPR43 expression in Hut78 and Jurkat cells were detected using RT-PCR,and IL-2 and IL-4 production in PMA/ionomycin stimulated T cells were measured by real-time PCR and ELISA. Also butyrate＇ s effect on cell calcium release was analyzed. The results showed that there were C-PR41, GPR43 expression in T cells and which were up-regulated by PMA stimulation. Butyrate induced calcium release, suppressed IL-2 production whereas enhanced IL-4 production. These effects of butyrate on T cells can not be inhibited by PTX. In addition, butyrate significantly suppressed MOG induced proliferation of T lymphocytes from EAE mice. In conclusion, butyrate regulates T cells mainly through its receptor GPR43, and has anti-inflammatory effect in EAE mice by inhibiting specific pro- inflammatory T cell proliferation.

关 键 词：丁酸钠 GPCR GPR43 T淋巴细胞 抗炎 

分 类 号：R962[医药卫生—药理学]