Department of Gastroenterology, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Shenyang, 110004, Liaoning, China.
Curr Microbiol. 2021 Apr;78(4):1543-1550. doi: 10.1007/s00284-021-02392-1. Epub 2021 Mar 6.
In this study, we treated HCT-116 cells with Clostridium butyricum (C. butyricum) supernatant and observed its effects on the TLR2/MyD88/NF-κB signaling pathway and RORγt, to further explore the possible immune regulatory mechanism of C. butyricum. Our results showed that C. butyricum supernatant downregulated the mRNA and protein levels of TLR2, MyD88, NF-κBp65, and RORγt in HCT-116 cells and the protein levels of phospho-NF-κBp65. Partial blockage of TLR2 by CD282 weakened the inhibitory effects of C. butyricum supernatant on the above pathway components. Those component levels were still inhibited by C. butyricum supernatant after Pam3CSK4 activation of TLR2. In summary, C. butyricum supernatant can inhibit the TLR2/MyD88/NF-κB signaling pathway and the expression of RORγt in HCT-116 cells. These effects are at least partly achieved through inhibition of TLR2.
在这项研究中，我们用丁酸梭菌（C. butyricum）上清液处理 HCT-116 细胞，观察其对 TLR2/MyD88/NF-κB 信号通路和 RORγt 的影响，进一步探讨 C. butyricum 的可能免疫调节机制。我们的结果表明，丁酸梭菌上清液下调了 HCT-116 细胞中 TLR2、MyD88、NF-κBp65 和 RORγt 的 mRNA 和蛋白水平，以及磷酸化 NF-κBp65 的蛋白水平。用 CD282 部分阻断 TLR2 减弱了丁酸梭菌上清液对上述通路成分的抑制作用。TLR2 被 Pam3CSK4 激活后，丁酸梭菌上清液仍能抑制上述成分的水平。总之，丁酸梭菌上清液可以抑制 HCT-116 细胞中的 TLR2/MyD88/NF-κB 信号通路和 RORγt 的表达。这些作用至少部分是通过抑制 TLR2 实现的。
