Clostridium butyricum CB1 up-regulates FcRn expression via activation of TLR2/4-NF-κB signaling pathway in porcine small intestinal cells.

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.