Anti-TRAF6 polyclonal antibody

Polysaccharides are closely associated with immune regulation. In this study, the aim was to investigate the effect of polysaccharides from Cordyceps gunnii mycelia (PPS) in cyclophosphamide (CTX)-induced immunodeficient mice. Compared with the CTX-induced immunosuppressed mice, the spleen and thymus indexes in mice with orally administered PPS were significantly increased, body weight loss was alleviated, and the natural killer (NK) cytotoxicity and proliferative activities of the lymphocytes were elevated. The recovery of peripheral white blood cells, red blood cells, hemoglobins and platelets was accelerated. Furthermore, the results from ELISA showed that PPS could up-regulate the serum levels of IL-2, IL-12, IFN-gamma and IgG, and reduce the level of TGF-beta. Histopathological analysis of the spleen revealed the protective effect of PPS against CTX-induced immunosuppression. Western blotting results showed that PPS possessed immunomodulatory activity via TLR4/TRAF6/NF-kappa B signalling pathways. Finally, the intestinal absorption of PPS was poor, as detected in the Caco-2 transwell system. Taken together, these findings suggest that PPS plays a crucial role in protection against immunosuppression in cyclophosphamide-treated mice and could be a potential candidate for use in immune therapy regimens.

The contribution of miRNA in the pathogenesis of ulcerative colitis (UC) has emerged in the past few decades. Differential miRNA expression has been demonstrated in UC patients, and their ability to target the genes involved in inflammatory pathway has also been explored in recent years. miR-125b and miR-223 have been demonstrated to get upregulated within the colonic mucosa of UC patients. Here, we explored the biological relevance of miR-125b and miR-223 altered expression during UC by identifying the potential gene targets for miR-125b and miR-223. TRAF6 and A20, the signaling molecules involved in the NF kappa B pathway, were identified as target genes for miR-125b while IKK alpha was identified as a gene target for miR-223. The colonic mucosal samples from UC patients exhibited a significant rise in miR-125b and miR-223 expression while a subsequent downregulation was observed in the expression of TRAF6, A20, and IKK alpha. This negative correlation between miRNAs and their respective target genes was validated by co-transfecting miR-125b and miR-223 in HT29 cells. Co-transfection with miR-125b resulted in a marked decline in the expression of TRAF6 and A20, while the miR-223 co-transfected cells exhibited lower IKK alpha expression levels. Additionally, co-transfection with miR-125b or miR-223 in HT29 cells caused higher p65 and pro-inflammatory cytokines (IL-8 and IL-1 beta) expression upon LPS stimulation. From our findings, we highlight the possible contribution of miR-125b and miR-223 in regulating the inflammatory response during UC by negatively regulating the expression of TRAF6, A20, and IKK alpha. Therefore, we conclude that these two miRNAs could be considered as potential candidates for developing promising biomarkers for screening and diagnosis of UC.