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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.v17.i2.70
pages 161-168

Armillaridin, a Honey Medicinal Mushroom, Armillaria mellea (Higher Basidiomycetes) Component, Inhibits Differentiation and Activation of Human Macrophages

Tsang-Pai Liu
Department of Surgery, Mackay Memorial Hospital, Mackay Junior College of Medicine, Nursing and Management, Department of Graduate Institute of Cancer Biology and Drug Medicine Taipei Medical University, Department of Medicine Mackay Medical College
Chien-Chih Chen
Department of Biotechnology, Hungkuang University, Taichung, Taiwan
Pei-Yu Shiao
Department of Medical Research, Mackay Memorial Hospital, Taipei, Taiwan
Hui-Ru Shieh
Department of Medical Research, Mackay Memorial Hospital, Taipei, Taiwan
Yu-Yawn Chen
Department and Graduate School of Physical Education, National Taiwan Sport University, Taichung, Taiwan
Yu-Jen Chen
Department of Medical Research, Mackay Memorial Hospital, Taipei, Taiwan; Department of Radiation Oncology, Mackay Memorial Hospital, Taipei, Taiwan; Graduate Institute of Pharmacology, Taipei Medical University, Taipei, Taiwan

ABSTRACT

Armillaridin (AM) is an aromatic ester compound isolated from honey medicinal mushroom, Armillaria mellea, which has anti-cancer potential. This study was designed to examine the effects of AM on differentiation and activation macrophages, the major ontogeny of innate immunity. Macrophages were derived from CD14+ monocytes which were sorted from human peripheral blood mononuclear cells. Cell viability was assessed by trypan blue exclusion test. Cells were stained with Liu's dye for observation of morphology. Expression of surface antigens was examined by flow cytometric analysis. Phagocytosis and generation of reactive oxygen species (ROS), as functional assays, were evaluated by counting engulfed yeasts and DCFH-DA reaction. The viability of macrophages was not significantly reduced by AM. AM at nontoxic concentrations markedly increased cytoplasmic vacuoles. The expression of surface CD14, CD16, CD36, and HLA-DR was suppressed. The phagocytosis function, but not ROS production, of macrophages was inhibited by AM. Armillaridin could inhibit the differentiation and activation of human macrophages. It may have potential to be developed as a biological response modifier for inflammatory diseases.