Immunostimulating and intracellular signaling pathways mechanism on macrophage of rhamnogalacturonan-I type polysaccharide purified from radish leaves

In this study, the intracellular signaling pathways involved in macrophage activation through the RG-I-type polysaccharide (REP-I) purified from radish leaves were elucidated. The gene expression and secretion of immune-related factors such as interleukin (IL)-6, tumor necrosis factor (TNF)-??, and nitrogen oxide (NO) from macrophages were enhanced by the addition of REP-I. Moreover, immunoblotting and immunocytochemistry analyses indicated that REP-I dose-dependently phosphorylated the mitogen-activated protein kinase (MAPK) and nuclear factor-??B (NF-??B) pathways. An investigation using different inhibitors revealed that the effect of REP-I on NO secretion was mostly promoted by c-Jun N-terminal kinase (JNK) and NF-??B. Furthermore, the secretion of IL-6 was mostly induced via extracellular-signal-regulated kinase (ERK), JNK, and NF-??B. TNF-?? secretion was mostly induced via NF-??B. In contrast, an investigation using anti-pattern recognition receptor (PRR) antibodies revealed that the effect of REP-I on the secretion of NO was mostly related with dectin-1, scavenger receptor (SR), toll-like receptor (TLR)2, TLR4, CD14, and CD11b. Furthermore, the secretion of IL-6 was mostly involved with SR, and the secretion of TNF-?? was mostly relevance to TLR2. In conclusion, it is affirmed that immunostimulatory activation of macrophage of REP-I purified from radish leaves was deeply associated with several PRR and phosphorylating MAPK and NF-??B.

Automated summary

This study elucidated the intracellular signaling pathways involved in macrophage activation by REP-I polysaccharide purified from radish leaves. REP-I enhanced the expression and secretion of immune-related factors in macrophages. The effects were mediated by phosphorylation of MAPK and NF-κB pathways, with different pathways involved in the secretion of different factors. The study also revealed the involvement of pattern recognition receptors in the effects of REP-I.