β-Glucan Induces Training Immunity to Promote Antiviral Activity by Activating TBK1

Guolei Wang; Zhiqiang Li; Mingfu Tian; Xianghua Cui; Jun'e Ma; Siyu Liu; Chenglin Ye; Li Yuan; Muhammad Suhaib Qudus; Uzair Afaq; Kailang Wu; Xinghui Liu; Chengliang Zhu

doi:10.3390/v15051204

β-Glucan Induces Training Immunity to Promote Antiviral Activity by Activating TBK1

Viruses. 2023 May 19;15(5):1204. doi: 10.3390/v15051204.

Authors

Affiliations

¹ Department of Clinical Laboratory, Institute of Translational Medicine, Renmin Hospital of Wuhan University, Wuhan 430060, China.
² State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, China.
³ Department of Clinical Laboratory, Zhongnan Hospital of Wuhan University, Wuhan 430060, China.
⁴ Department of Clinical Laboratory, Shanghai Gongli Hospital, The Second Military Medical University, Pudong New Area, Shanghai 200135, China.

Abstract

Many studies have shown that β-glucan induces a trained immune phenotype in innate immune cells to defend against bacterial and fungal infections. The specific mechanism involves cellular metabolism and epigenetic reprogramming. However, it is unclear whether β-glucan plays a role in antiviral infection. Therefore, this study investigated the role of trained immunity induced by Candida albicans and β-glucan in antiviral innate immunity. It showed that C. albicans and β-glucan promoted the expression of interferon-β (IFN-β) and interleukin-6 (IL-6) in mouse macrophages triggered by viral infection. In addition, β-glucan pretreatment attenuated the pathological damage induced by the virus in mouse lungs and promoted the expression of IFN-β. Mechanistically, β-glucan could promote the phosphorylation and ubiquitination of TANK Binding Kinase 1 (TBK1), a key protein of the innate immune pathway. These results suggest that β-glucan can promote innate antiviral immunity, and this bioactive material may be a potential therapeutic target for antiviral treatment.

Keywords: TBK1; innate immunity; trained immunity; ubiquitination.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Animals
Antiviral Agents* / pharmacology
Immunity, Innate
Interferon-beta / genetics
Mice
Phosphorylation
Protein Serine-Threonine Kinases / metabolism
Signal Transduction*

Substances

Antiviral Agents
Interferon-beta
Tbk1 protein, mouse
Protein Serine-Threonine Kinases

Grants and funding

The Fundamental Research Funds for the Central Universities (No. 2042022kf1215), the Special Funds for Innovation in Scientific Research Program of Zhongshan under Grant 2020AG024, the Clinical Research Project of Health Industry of Shanghai Municipal Health Commission (grant no. 202140407), the Key Disciplines Group Construction Project of Pudong Health Bureau of Shanghai (Grant No. PWZxq2022-08), Chinese foundation for hepatitis prevention and control-TianQing liver disease research fund subject (TGQB20210109), the Open Funds of Key Laboratory of Diagnosis and Treatment of Digestive System Tumors of Zhejiang Province (KFJJ-202005, KFJJ-201907), the Open Research Program of the State Key Laboratory of Virology of China (2021KF002, 2021KF006). The Open Research Program of the State Key Laboratory of Virology of China (2022KF003).