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International Journal of Medicinal Mushrooms
Fator do impacto: 1.423 FI de cinco anos: 1.525 SJR: 0.431 SNIP: 0.661 CiteScore™: 1.38

ISSN Imprimir: 1521-9437
ISSN On-line: 1940-4344

Volumes:
Volume 21, 2019 Volume 20, 2018 Volume 19, 2017 Volume 18, 2016 Volume 17, 2015 Volume 16, 2014 Volume 15, 2013 Volume 14, 2012 Volume 13, 2011 Volume 12, 2010 Volume 11, 2009 Volume 10, 2008 Volume 9, 2007 Volume 8, 2006 Volume 7, 2005 Volume 6, 2004 Volume 5, 2003 Volume 4, 2002 Volume 3, 2001 Volume 2, 2000 Volume 1, 1999

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

RESUMO

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.


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