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Published on: January 7, 2019
Immune enhancing effect of a Maillard-type lysozyme-galactomannan conjugate via signaling pathways
Young-min Ha1, Su-Hyun Chun, Seung-taek Hong
1Division of Food Bioscience and Technology, College of Life Sciences and Biotechnology, Korea University, Seoul 136-701, Republic of Korea.
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.
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.
