中文摘要：

背景：Faecalibacterium prausnitzii（F.prausnitzii）在炎症性肠病（IBD）患者肠道内减少，与IBD发生有一定相关性。目的：研究Fprausnitzii及其产物体外对大鼠脾细胞分泌促炎因子白细胞介素（IL）-17的抑制作用和机制。方法：以IL-6、转化生长因子（TGF）-B或骨髓来源树突细胞（BMDC）分别刺激大鼠脾细胞。将脾细胞分为阳性对照组、Fprausnitzii上清液组、Fprausnitzii组、长双歧杆菌组、丁酸钠组，以未进行任何干预的脾细胞作为阴性对照。以ELISA法检测细胞培养液中IL-10、IL-12、IL-17、IL-23含量。结果：以细胞因子或BMDC刺激后，与阴性对照组相比，阳性对照组脾细胞IL-17含量均明显升高[（309．24±21．30）pg／mL对（182．20±89．12）pg／mL；（20．54±2．12）pg／mL对（17．36±0．38）pg／mL]（P〈0．05）。与阳性对照组相比，Fprausnitzii上清液可明显抑制细胞因子或BMDC诱导的脾细胞IL-17含量[（58．11±19．20）pg／mL对（309．24±21．30）pg／mL；（17．25±0．42）pg／mL对（20．54±2．12）pg/mL]（P〈0．05）。结论：Fprausnitzii可通过其产物调节免疫反应，可能与抑制Th17细胞活化有关。

英文摘要：

Background： Faecalibacterium prausnitzii （F. prausnitzii） is decreased in patients with inflammatory bowel disease （ IBD ） , and has some correlation with the development of IBD. Aims： To investigate the suppressive effect and mechanism of F. prausnitzii and products on proinflammatory factor interleukin （IL） -17 secretion in rat splenocytes in vitro. Methods： Rat splenocytes were stimulated by IL-6 plus transforming growth factor （TGF）-13 or bone marrow derived dendritic cell （BMDC）. Splenocytes were divided into positive control group, F. prausnitzii supernatant group, F. prausnitzii group, Bifidobacterium longum group, butyrate sodium group. Splenocytes without intervention were served as negative controls. Concentrations of IL-10, IL-12, IL-17, IL-23 in cell culture medium were determined by ELISA. Results： After stimulated by cytokines or BMDC and compared with negative control group, IL-17 concentration in splenocytes in positive control group was significantly increased [ （309.24 ± 21.30） pg/mL vs. （ 182.20 ± 89.12） pg/mL ; （20.54 ± 2.12） pg/mL vs. （ 17.36 ± 0.38） pg/mL] （P 〈 0.05）. Compared with positive control group, F. prausnitzii supernatant could significantly inhibit IL-17 concentration induced by cytokines or BMDC [ （58. 11 ± 19.20） pg/mL vs. （309.24 ±21.30） pg/mL; （ 17.25 ± 0.42） pg/mL vs. （20.54 ± 2.12） pg/mL] （ P 〈 0.05 ）. Conclusions ： F. prausnitzii products can regulate the immune response by inhibiting the activation of Thl7 cells.