TRAF6 and inflammatory bowel disease: Since activation of TLR4/Myd88/TRAF6 signaling triggers the downstream cascades involved in IBD pathogenesis and that the TLR4 receptor possesses a high affinity for many exogenous ligands of natural origin [17], based on previous results, we hypothesized that the modulation of immuno-inflammatory pathways by Ulva pertusa could be related to TLR4/Myd88-dependent signaling downregulation.