Role of Baicalin in Anti-Influenza Virus A as a Potent Inducer of IFN-Gamma.

Ming Chu,Ming-Bo Zhang,Zheng-Yun Chu,Yue-Dan Wang,Lan Xu

doi:10.1155/2015/263630

Abstract

Baicalin (BA) is a flavonoid compound purified from Scutellaria baicalensis Georgi and has been shown to possess a potent inhibitory activity against viruses. However, the role of BA in anti-influenza virus has not been extensively studied, and the immunological mechanism of BA in antiviral activity remains unknown. Here, we observed that BA could protect mice from infection by influenza virus A/PR/8/34 (H1N1), associated with increasing IFN-γ production, but presented no effects in IFN-γ or IFN-γ receptor deficient mice. Further study indicated that BA could inhibit A/PR/8/34 replication through IFN-γ in human PBMC. Moreover, BA can directly induce IFN-γ production in human CD4+ and CD8+ T cells and NK cells, and activate JAK/STAT-1 signaling pathway. Collectively, BA exhibited anti-influenza virus A (H1N1) activity in vitro and in vivo as a potent inducer of IFN-γ in major IFN-γ producing cells.

Highlights

Influenza is one of the most common respiratory diseases in human and is potentially lethal in immunocompromised persons
To further systematic investigate the anti-influenza activity of BA, we examined its effect on mouse-adapted strain of human influenza virus A/PR/8/34 in mice
We first extracted the compound of Scutellaria baicalensis Georgi and examined its antiviral activity against a mouse-adapted influenza virus A/FM/1/47

Summary

Introduction

Influenza is one of the most common respiratory diseases in human and is potentially lethal in immunocompromised persons. It affects all types of people, from infants to the elderly, and is usually caused by influenza virus A and influenza virus B. IFN response represents an early host defense event, one that occurs prior to the onset of the adaptive immune response, produced both in the early stages of infection by NK cells and at later stages by activated CD4+ and CD8+ T cells [6]. The innate immune response to viral infection depends on the integrity of this network of cytokines, which is tightly regulated [7]

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Results

Conclusion