Immune enhancing effect of a Maillard-type lysozyme-galactomannan conjugate via signaling pathways

Abstract

We studied the immune-modulating effect of Maillard-type lysozyme-galactomannan conjugate (LGC). LGC significantly induced nitric oxide, and expressions of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-8 on the murine macrophage Raw 264.7 cell line. In the mechanism of LGC, while extracellular signal-regulated kinase (ERK) was important for the induction of TNF-α, IL-1β and IL-8, the phosphorylation of C-Jun NH2-termianl kinase (JNK) contributed to the induction of TNF-α and IL-1β to a greater degree. These cytokines were less sensitive to the inhibition of p38. Nuclear factor (NF)-κB was involved in the induction of TNF-α and IL-1β. These data indicate that LGC has immune-modulating effects via JNK, ERK and NF-κB pathways, and that LGC may contribute to host immune defense.

Keywords: 3-(4,5-dimethylthazol-2-yl)-2,5-diphenyl tetrazolium bromide; C-Jun NH2-termianl kinase; DMEM; Dulbecco's modified Eagle's medium; ECL; ERK; FBS; G; Galactomannan; IFN-γ; IL; Immune-modulating effect; JNK; L; LGC; Lysozyme; MAPKs; MTT; Maillard reaction; NF-κB; NO; PVDF; RH; TGF-β; TNF-α; electrochemiluminescent; extracellular signal-regulated kinase; fetal bovine serum; galactomannan; iNOS; inducible nitric oxide synthase; interferon-γ; interleukin; lysozyme; lysozyme-galactomannan conjugate; mitogen-activated protein kinases; nitric oxide; nuclear factor-κB; polyvinylidene difluoride; relative humidity; transforming growth factor-β; tumor necrosis factor.