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, Yuan Li, Muhammad Suhaib Qudus, Uzair Afaq, Kailang Wu, Xinghui Liu, Chengliang Zhu
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.