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Phagocytic effects of β‐glucan from Coriolus versicoloar are related with Dectin‐1 signaling and NOS and Ikaros regulation in macrophages
Author(s) -
Park Sulkyoung,
Jang SeonA,
Lim Jung Dae,
Sohn Eun Soo,
Kang Nam Sung,
Pyo Suhkneung,
Sohn Eun Hwa
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.1003.9
Subject(s) - laminarin , phagocytosis , glucan , microbiology and biotechnology , receptor , chemotaxis , immune system , chemistry , biology , biochemistry , polysaccharide , immunology
The β‐glucan receptor dectin‐1 may contribute to phagocytosis. Coriolus versicolor has been known to have immunomodulatory effects. For further understanding of the phagocytic activity and mechanisms for β‐glucan from C. versicolor, we examined phagocytosis, NO and NOS production in β‐glucan‐treated macrophages by dectin‐1 antagonist, laminarin. It showed that the treatment of β‐glucan induced a remarkable increase of phagocytosis in RAW264.7 cells, peritoneal macrophages and microglia. However, the activity of β‐glucan‐induced phagocytosis was abrogated by the pre‐treatment of laminarin. We also examined whether NO production and NOS expression are involved in phagocytosis and β‐glucan induced dectin‐1 signal pathways. Our results showed that phagocytic activity was not increased in the presence of iNOS inhibitor, S‐methylisothiourea, cNOS inhibitor and diphenylene iodonium chloride in the β‐glucan‐treated cells. The role of Ikaros in regulating phagocytic effects of β‐glucan were also determined. Taken together, these results suggest that β‐glucan enhances phagocytosis via dectin‐1 signal pathways and these effects of β‐glucan might be related to NO, cNOS, iNOS and Ikaros regulation.