TRIF is essential for the anti-inflammatory effects of Astragalus polysaccharides on LPS-infected Caco2 cells.

As an immune-regulator, Astragalus polysaccharides (APS) could effectively modulate the activity of toll-like receptor 4 (TLR4) signaling pathway, and induce anti-inflammatory response in intestinal. Our research before indicated that toll/interleukin 1 receptor-domain-containing adapter-inducing interferon-b (TRIF) might be a critical regulator for APS. So, in this experiment, we analyzed the effects of APS on lipopolysaccharide (LPS)-infected Caco2 cells in the circumstances of TRIF knockout. By using qRT-PCR and flow cytometry method, we analyzed the genes expression at transcriptional and translational level, respectively. The results of genes expression at both transcription and translation level showed that LPS could activate the myeloid differentiation factor 88 (MyD88)-TNF receptor associated factor (TRAF) pathway downstream from TLR4, and induce the high expression of pro-inflammatory cytokines. However, APS could effectively suppress the LPS induced inflammatory response. While, in the context of TRIF knockout, APS couldn't effectively attenuate the LPS activated MyD88-TRAF6 pathway, as well as the expression of pro-inflammatory cytokines. Above all, we concluded that APS could antagonize the LPS induced inflammatory response by a TRIF-dependent manner.