Novel Fatty Acid in Cordyceps Suppresses Influenza A (H1N1) Virus-Induced Proinflammatory Response Through Regulating Innate Signaling Pathways

Run-Feng Li; Xiao-Bo Zhou; Hong-Xia Zhou; Zi-Feng Yang; Hai-Ming Jiang; Xiao Wu; Wen-Jia Li; Jian-Jian Qiu; Jia-Ning Mi; Ming Chen; Nan-Shan Zhong; Guo-Yuan Zhu; Zhi-Hong Jiang

doi:10.1021/acsomega.0c05264

Novel Fatty Acid in Cordyceps Suppresses Influenza A (H1N1) Virus-Induced Proinflammatory Response Through Regulating Innate Signaling Pathways

ACS Omega. 2021 Jan 7;6(2):1505-1515. doi: 10.1021/acsomega.0c05264. eCollection 2021 Jan 19.

Authors

Run-Feng Li¹, Xiao-Bo Zhou¹, Hong-Xia Zhou², Zi-Feng Yang^{3

1

4

5}, Hai-Ming Jiang³, Xiao Wu³, Wen-Jia Li⁶, Jian-Jian Qiu⁶, Jia-Ning Mi¹, Ming Chen¹, Nan-Shan Zhong^{3

1}, Guo-Yuan Zhu¹, Zhi-Hong Jiang¹

Affiliations

¹ State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau (SAR) 519020, China.
² Dongguan People's Hospital, Dongguan 523000, China.
³ State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou 510120, China.
⁴ KingMed Virology Diagnostic & Translational Center, Guangzhou 510000, China.
⁵ Guangdong-Hong Kong-Macao Joint Laboratory of Infectious Respiratory Disease, Guangzhou 510000, China.
⁶ Dongguan HEC Cordyceps R&D Co.,Ltd, Dongguan 523850, China.

Abstract

Influenza virus (IV) infections usually cause acute lung injury characterized by exaggerated proinflammatory responses. The paucity of therapeutic strategies that target host immune response to attenuate lung injury poses a substantial challenge in management of IV infections. In this study, we chemically synthesized a novel fatty acid (2Z,4E)-deca-2,4-dienoic acid (DDEA) identified from Chinese Cordyceps by using UHPLC-Q-TOF-MS techniques. The DDEA did not inhibit H1N1 virus replication but attenuated proinflammatory responses by reducing mRNA and protein levels of TNF-α, IFN-α, IFN-β, IL-6, CXCL-8/IL-8, CCL-2/MCP-1, CXCL-10/IP-10, CCL-3/MIP-1α, and CCL-4/MIP-1β in A549 cells and U937-derived macrophages. The anti-inflammatory effect occurred through downregulations of TLR-3-, RIG-I-, and type I IFN-activated innate immune signaling pathways. Altogether, our results indicate that DDEA may potentially be used as an anti-inflammatory therapy for the treatment of IV infections.