Abstract

Objective We wished to investigate the effects of the traditional Chinese medicine Gui Zhi Ma Huang Ge Ban Tang on controlling influenza A virus (IAV) infection and improving inflammation in mouse lungs. Method Mice were maintained in normal and cold environments and infected with IAV by intranasal application, respectively. Real-time quantitative polymerase chain reaction was used to measure mRNA expression of TLR7, myeloid differentiation primary response 88 (MyD88), and nuclear factor-kappa B (NF-κB)p65 in the TLR7 signaling pathway and virus replication in lungs. Western blotting was used to measure expression levels of TLR7, MyD88, and NF-κB p65 proteins. Flow cytometry was used to detect the proportion of T-helper (Th)1/Th2 and Th17/T-regulatory (Treg) cells. Results Application of Gui Zhi Ma Huang Ge Ban Tang in influenza-infected mice in a cold environment showed (i) downregulation of TLR7, MyD88, and NF-κBp65; (ii) inhibition of transcriptional activities of promoters coding for TLR7, MyD88, and NF-κBp65; (iii) reduction in the proportion of Th1/Th2 and Th17/Treg cells. Conclusions Gui Zhi Ma Huang Ge Ban Tang had a good therapeutic effect on mice infected with IAV, especially in the cold environment. It could reduce lung inflammation in mice significantly and elicit an anti-influenza effect by downregulating expression of the key factors in TLR7 signaling pathway.

Highlights

  • The influenza A virus (IAV) is an important pathogen in the respiratory tract that causes seasonal epidemics and pandemics of considerable morbidity and mortality [1, 2] IAV infection induces the host’s natural immune response [3] and activation of a Toll-like receptor- (TLR-) mediated antiviral signaling pathway

  • Ribavirin [6] and oseltamivir [7, 8] are effective in suppressing viral replication in IAV infection, but the IAV is susceptible to variation

  • Using yinqiaosan and xinjiaxiangruyin as controls, we investigated the effects of Gui Zhi Ma Huang Ge Ban Tang on the TLR7 signaling pathway and on the immune balance of T cells in mouse lungs infected with the IAV in a cold environment

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Summary

Introduction

The influenza A virus (IAV) is an important pathogen in the respiratory tract that causes seasonal epidemics and pandemics of considerable morbidity and mortality [1, 2] IAV infection induces the host’s natural immune response [3] and activation of a Toll-like receptor- (TLR-) mediated antiviral signaling pathway. The TLR family plays an important part in pathogen recognition and activation of innate immunity [4]. Current vaccines are not highly protective if antigenically different new strains emerge, such as the outbreak of the pandemic (H1N1) 2009 virus [9, 10]. Finding a measure that protects against the emergence of an unexpected influenza strain is highly desirable

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