Joo Y. Lee

TL;DR: A novel mechanism by which fatty acids modulate signaling pathways and target gene expression is represented by both SFA-induced COX-2 expression and its inhibition by UFAs are mediated through a common signaling pathway derived from Tlr4.

TL;DR: Results demonstrate that inhibition of COX-2 expression by n-3 PUFAs is mediated through the modulation of TLR-mediated signaling pathways, and the beneficial or detrimental effects of different types of dietary fatty acids on the risk of the development of many chronic inflammatory diseases may be in part mediated throughThe modulation ofTLRs.

TL;DR: It is demonstrated that lauric acid activates TLR2 dimers as well as TLR4 for which respective bacterial agonists require acylated fatty acids, whereas DHA inhibits the activation of all TLRs tested.

TL;DR: The results suggest that saturated and polyunsaturated fatty acids reciprocally modulate the activation of TLR4 and its downstream signaling pathways involving MyD88/IRAK/TRAF6 and PI3K/AKT and further suggest the possibility thatTLR4-mediated target gene expression and cellular responses are also differentially modulated by saturated and uns saturated fatty acids.

TL;DR: The results presented in this study demonstrate that the saturated fatty acid, lauric acid, up-regulates the expression of costimulatory molecules, MHC class II, and cytokines in bone marrow-derived DCs, implying that TLRs are involved in sterile inflammation and immune responses induced by nonmicrobial endogenous molecules.