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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。
Short chain fatty acids are commonly produced by the fermentation of food fibers by gut microbes and have been reported to play an important role in immunity and inflammation. This article studies the role of sodium butyrate in the regulation of T lymphocytes through its receptor GPR43, and explores the anti-inflammatory effects and mechanisms of sodium butyrate on T cells. The expression of GPR41 and GPR43 in T cells was detected by RT-PCR using Hut78 and Jurkat cell lines as models. The levels of IL-2 and IL-4 in PMA / Ionomycin-induced T lymphocytes treated with sodium butyrate were detected by real-time fluorescence quantitative PCR and verified by ELISA and other methods. To investigate the specific mechanism and target of sodium butyrate on T cells by RT-PCR and intracellular calcium detection. The results showed that GPR41 and GPR43 were expressed in T cells and significantly increased after PMA stimulation. Sodium butyrate can stimulate the release of intracellular calcium, inhibit IL-2 and promote the production of IL-4, and this regulation is not affected by Gαi inhibitor PTX. In addition, sodium butyrate can significantly inhibit MOG-induced proliferation of spleen lymphocytes of EAE mice in vitro. These results indicate that sodium butyrate modulates the production of cytokines mainly through GPR43 receptors in T lymphocytes and inhibits the proliferation of inflammatory T lymphocytes to exert their anti-inflammatory function.