The neonatal Fc receptor (FcRn) mediates the bidirectional transport of immunoglobulin G (IgG) across hyperpolarized epithelial cells. Overexpression of FcRn increases serum IgG and humoral immune response. Probiotics can improve the host’s serum and intestinal mucosal IgG. However, whether probiotics regulate FcRn and its specific mechanism are still unclear. Our research showed that heat inactivated Clostridium butyricum CB1 (heat-inactivated CB1) up-regulated FcRn expression in porcine small intestinal epithelial (IPI-2I) cells. Furthermore, heat-inactivated CB1 stimulation activated the nuclear factor kappa B (NF-κB) signaling pathway. Moreover, FcRn expression decreased after blocking the NF-κB signaling pathway by NF-κB inhibitor BAY11-7028, suggesting that heat-inactivated CB1 induced FcRn expression via the NF-κB signaling pathway. Using small interfering RNAs (siRNAs), we found that knockdown of TLR2/4, MyD88 and TRIF reduced NF-κB activity induced by heat-inactivated CB1, as well as up-regulation of FcRn expression after heat-inactivated CB1 stimulation. Taken together, our data indicated that heat-inactivated CB1 up-regulated FcRn expression via TLR2/4-MyD88/TRIF-NF-κB signaling pathway. These results provided a new perspective for us to understand the enhancement of C. butyricum on intestinal mucosal immunity.

新生儿 Fc 受体 (FcRn) 介导免疫球蛋白 G (IgG) 通过超极化上皮细胞的双向转运。FcRn 的过表达增加血清 IgG 和体液免疫反应。益生菌可以提高宿主的血清和肠黏膜IgG。然而，益生菌是否调节FcRn及其具体机制尚不清楚。我们的研究表明，热灭活丁酸梭菌CB1（热灭活的 CB1）上调猪小肠上皮 (IPI-2I) 细胞中的 FcRn 表达。此外，热灭活的 CB1 刺激激活了核因子 kappa B (NF-κB) 信号通路。此外，通过 NF-κB 抑制剂 BAY11-7028 阻断 NF-κB 信号通路后，FcRn 表达降低，表明热灭活的 CB1 通过 NF-κB 信号通路诱导 FcRn 表达。使用小干扰 RNA (siRNA)，我们发现 TLR2/4、MyD88 和 TRIF 的敲低降低了热灭活 CB1 诱导的 NF-κB 活性，以及​​热灭活 CB1 刺激后 FcRn 表达的上调。总之，我们的数据表明热灭活的 CB1 通过 TLR2/4-MyD88/TRIF-NF-κB 信号通路上调 FcRn 表达。C. butyricum对肠黏膜免疫的影响。