title: Hirsutella sinensis mycelium suppresses interleukin-1β and interleukin-18 secretion by inhibiting both canonical and non-canonical inflammasomes.
abstract: Cordyceps sinensis is a medicinal mushroom used for centuries in Asian countries as a health supplement and tonic. Hirsutella sinensis-the anamorphic, mycelial form of C. sinensis-possesses similar properties, and is increasingly used as a health supplement. Recently, C. sinensis extracts were shown to inhibit the production of the pro-inflammatory cytokine IL-1β in lipopolysaccharide-treated macrophages. However, the molecular mechanism underlying this process has remained unclear. In addition, whether H. sinensis mycelium (HSM) extracts also inhibit the production of IL-1β has not been investigated. In the present study, the HSM extract suppresses IL-1β and IL-18 secretion, and ATP-induced activation of caspase-1. Notably, we observed that HSM not only reduced expression of the inflammasome component NLRP1 and the P2X7R but also reduced the activation of caspase-4, and ATP-induced ROS production. These findings reveal that the HSM extract has anti-inflammatory properties attributed to its ability to inhibit both canonical and non-canonical inflammasomes.
authors: Center for Molecular and Clinical Immunology, Chang Gung University, Taoyuan, Taiwan, Republic of China.
authors: Tsung-Teng
authors: TT
authors: Huang
authors: Kowit-Yu
authors: KY
authors: Chong
authors: David M
authors: DM
authors: Ojcius
authors: Yi-Hui
authors: YH
authors: Wu
authors: Yun-Fei
authors: YF
authors: Ko
authors: Cheng-Yeu
authors: CY
authors: Wu
authors: Jan
authors: J
authors: Martel
authors: Chia-Chen
authors: CC
authors: Lu
authors: Hsin-Chih
authors: HC
authors: Lai
authors: John D
authors: JD
authors: Young
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000494:pharmacology; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism; D001203:Ascomycota / Q000378:metabolism*; D020169:Caspases / Q000378:metabolism; D015536:Down-Regulation / Q000187:drug effects; D004789:Enzyme Activation / Q000187:drug effects; D000431:Ethanol; D006801:Humans; D058847:Inflammasomes / Q000037:antagonists & inhibitors* / Q000378:metabolism; D020382:Interleukin-18 / Q000235:genetics / Q000378:metabolism*; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008262:Macrophage Activation / Q000187:drug effects; D008264:Macrophages / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism / Q000382:microbiology; D008954:Models, Biological; D025282:Mycelium / Q000378:metabolism*; D000070576:NLR Proteins; D017382:Reactive Oxygen Species / Q000378:metabolism; D058848:Receptors, Purinergic P2X4 / Q000378:metabolism; D058486:Receptors, Purinergic P2X7 / Q000378:metabolism
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D051017:Apoptosis Regulatory Proteins; D058847:Inflammasomes; D020382:Interleukin-18; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D000070576:NLR Proteins; C427903:NLRP1 protein, human; D017382:Reactive Oxygen Species; D058848:Receptors, Purinergic P2X4; D058486:Receptors, Purinergic P2X7; D000431:Ethanol; D000255:Adenosine Triphosphate; D020169:Caspases