We investigated effects of tyrosol on upstream pathway regulating lipopolysaccharide (LPS)-induced inflammatory response, including cluster of differentiation 14 (CD14)-mediated LPS–macrophage binding, toll-like receptor 4 (TLR4)/myeloid differentiation factor 2 (MD2) expression and subsequent myeloid differentiation primary response gene 88 (MyD88) and TIR-domain-containing adapter-inducing interferon-β (TRIF) recruitments. Flow cytometry revealed that, compared with LPS-treated RAW264.7 cells (LPS group), those treated with LPS and tyrosol (1.2 mM) [LPS+T(1.2) group] demonstrated lower LPS–macrophage binding and membrane-bound CD14 (mCD14) and TLR4/MD2 expression (all p < 0.05). Immunoprecipitation/immunoblotting assay revealed lower MyD88 and TRIF concentrations in the LPS+T(1.2) group than in the LPS group (both p < 0.05). Soluble CD14 concentration was higher in the LPS+T(1.2) group than in the LPS group (p = 0.013); protease inhibition counteracted this effect. Thus, tyrosol inhibits LPS–macrophage binding, mCD14 and TLR4/MD2 expression, and MyD88 and TRIF recruitment, all possibly by enhancing protease-mediated mCD14 cleavage.
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