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
Summary
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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