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

Many studies have shown that beta-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 beta-glucan plays a role in antiviral infection. Therefore, this study investigated the role of trained immunity induced by Candida albicans and beta-glucan in antiviral innate immunity. It showed that C. albicans and beta-glucan promoted the expression of interferon- beta (IFN-beta) and interleukin-6 (IL-6) in mouse macrophages triggered by viral infection. In addition, beta-glucan pretreatment attenuated the pathological damage induced by the virus in mouse lungs and promoted the expression of IFN-beta. Mechanistically, figlucan could promote the phosphorylation and ubiquitination of TANK Binding Kinase 1 (TBK1), a key protein of the innate immune pathway. These results suggest that beta-glucan can promote innate antiviral immunity, and this bioactive material may be a potential therapeutic target for antiviral treatment.

Automated summary

Several studies have demonstrated that beta-glucan can induce trained immunity in innate immune cells to defend against bacterial and fungal infections, but its role in antiviral infection remains unclear. This study investigated the role of trained immunity induced by Candida albicans and beta-glucan in antiviral innate immunity. It showed that C. albicans and beta-glucan promoted the expression of IFN-beta and IL-6 in mouse macrophages triggered by viral infection. Mechanistically, beta-glucan could promote the phosphorylation and ubiquitination of TBK1, a key protein of the innate immune pathway. These findings suggest that beta-glucan can enhance innate antiviral immunity and may serve as a potential therapeutic target for antiviral treatment.