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International Journal of Medicinal Mushrooms
IF: 1.423 5-Year IF: 1.525 SJR: 0.431 SNIP: 0.661 CiteScore™: 1.38

ISSN Print: 1521-9437
ISSN Online: 1940-4344

International Journal of Medicinal Mushrooms

DOI: 10.1615/IntJMedMushrooms.2017024620
pages 957-965

Activation of NADPH Oxidase by β-Glucan from Phellinus baumii (Agaricomycetes) in RAW 264.7 Cells

Soo Kyung Sung
Department of Life Science, University of Seoul, Seoul, Korea
Sainkhuu Batbayar
Department of Life Science, University of Seoul, Seoul, Korea
Dong Hee Lee
Department of Life Sciences, University of Seoul, Seoul, Korea
Ha Won Kim
Department of Life Sciences, University of Seoul Dongdaemun-gu, Jennong-dong 90, Seoul 130-743, South Korea


Production of oxygen-derived free radicals in phagocytes is important in preventing bacterial and fungal infections. Among free radicals, superoxide anions are a typical reactive oxygen species secreted by macrophages and neutrophils. NADPH oxidase (NOX) is a key producer of superoxide anions in these cells. β-glucans from mushrooms modulate the immune system by binding with the dectin-1 receptor on macrophages. Dectin-1 functions as a pattern recognition receptor that recognizes the pathogen-associated molecular pattern of β-glucans. During dectin-1 signaling, NOX functions in the activated macrophages to produce ROS, which are critical in antimicrobial host defense. In this study, NOX activation was measured using a lucigenin chemiluminescence assay in RAW 264.7 murine macrophages treated for 1 hour with a β-glucan fraction from Phellinus baumii (BGF; 10, 100, 500, and 1000 μg/mL) in the absence or presence of phorbol 12-myristate 13-acetate (PMA) or lipopolysaccharide (LPS). NOX was activated at BGF concentrations exceeding 10 μg/mL. BGF in the presence of PMA or LPS activated the enzyme more than treatment with PMA or LPS alone. In the presence of the NOX inhibitor diphenyleneiodonium, BGF still activated NOX. When macrophages were treated with BGF and Staphylococcus aureus, bacterial viability was reduced in a concentration-dependent manner, possibly as a result of increased phagocytosis and oxygen radical production by the activated NOX. These results demonstrate that BGF is a potent stimulator of NOX in macrophages and augments macrophage-mediated phagocytosis and NOX activity.