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Eicosapentaenoic acid suppresses TRIF‐dependent signaling pathway of TLRs by targeting TBK1
Author(s) -
Shin HyeonMyeong,
Shim HyunJin,
Kim AhYeon,
Lee Yoo Jung,
Nam Hyeonjeong,
Youn HyungSun
Publication year - 2018
Publication title -
journal of food biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.507
H-Index - 47
eISSN - 1745-4514
pISSN - 0145-8884
DOI - 10.1111/jfbc.12490
Subject(s) - trif , irf3 , tank binding kinase 1 , tlr3 , interferon regulatory factors , signal transduction , tlr4 , toll like receptor , innate immune system , eicosapentaenoic acid , microbiology and biotechnology , receptor , biology , polyunsaturated fatty acid , chemistry , biochemistry , fatty acid , mapk/erk pathway , map kinase kinase kinase
Toll‐like receptors (TLRs) induce an innate immune system. In general, there are two main pathways in TLRs: the myeloid differentiation primary response protein 88 (MyD88)‐dependent and toll‐interleukin‐1 receptor domain‐containing adapter‐inducing interferon‐β (TRIF)‐dependent pathways. In this study, it has been investigated whether eicosapentaenoic acid (EPA), a polyunsaturated fatty acid (PUFA), and arachidic acid (ACA), a saturated fatty acid (SFA), can modulate the TLR signaling pathways. EPA suppressed the activation of interferon regulatory factor 3 (IRF3) and the expression of Interferon gamma‐induced protein (IP‐10) induced by Toll‐like receptor 3 (TLR3) or TLR4 agonists by targeting TANK‐binding kinase 1 (TBK1); however, ACA did not. These results demonstrate that EPA inhibits the TRIF‐dependent signaling in the TLR3 and TLR4 pathways. The results raise the possibility that certain dietary PUFAs can modulate TLR‐derived signaling and inflammatory target gene expression and can alter the susceptibility to microbial infection and chronic inflammatory diseases. Practical application Eicosapentaenoic acid (EPA) is a bioactive lipid that modulates inflammation and immunity. TLRs play a central role as initiators of the innate immune responses. EPA regulates TRIF‐dependent pathways of TLRs by targeting TBK1. EPA may be a useful strategy to understand the mechanism of antiinflammatory activities.