Dendritic Cell Activation by Glucan Isolated from Umbilicaria Esculenta.
- Author:
Hyung Sook KIM
1
;
Jee Youn KIM
;
Hong Kyung LEE
;
Moo Sung KIM
;
Sang Rin LEE
;
Jong Soon KANG
;
Hwan Mook KIM
;
Kyung Ae LEE
;
Jin Tae HONG
;
Youngsoo KIM
;
Sang Bae HAN
Author Information
- Publication Type:Original Article
- Keywords: Umbilicaria esculenta; Glucan; Dendritic cells; MAPKs; NF-kappaB
- MeSH: Dendritic Cells; Endocytosis; Glucans; Interleukin-12; Lichens; Lymphocyte Culture Test, Mixed; NF-kappa B; p38 Mitogen-Activated Protein Kinases; Phenotype; Phosphorylation; Polymyxin B; T-Lymphocytes; Tumor Necrosis Factor-alpha
- From:Immune Network 2010;10(6):188-197
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND: Lichen-derived glucans have been known to stimulate the functions of immune cells. However, immunostimulatory activity of glucan obtained from edible lichen, Umbilicaria esculenta, has not been reported. Thus we evaluated the phenotype and functional maturation of dendritic cells (DCs) following treatment of extracted glucan (PUE). METHODS: The phenotypic and functional maturation of PUE-treated DCs was assessed by flow cytometric analysis and cytokine production, respectively. PUE-treated DCs was also used for mixed leukocyte reaction to evaluate T cell-priming capacity. Finally we detected the activation of MAPK and NF-kappaB by immunoblot. RESULTS: Phenotypic maturation of DCs was shown by the elevated expressions of CD40, CD80, CD86, and MHC class I/II molecules. Functional activation of DCs was proved by increased cytokine production of IL-12, IL-1beta, TNF-alpha, and IFN-alpha/beta, decreased endocytosis, and enhanced proliferation of allogenic T cells. Polymyxin B, specific inhibitor of lipopolysaccharide (LPS), did not affect PUE activity, which suggested that PUE was free of LPS contamination. As a mechanism of action, PUE increased phosphorylation of ERK, JNK, and p38 MAPKs, and enhanced nuclear translocation of NF-kappaB p50/p65 in DCs. CONCLUSION: These results indicate that PUE induced DC maturation via MAPK and NF-kappaB signaling pathways.
