Abstract
Objective: The objective of this study was to observe the effects of forsythoside A on controlling influenza A virus (IAV) infection and improving the prognosis of IAV infection. Methods: Forty-eight SPF C57BL/6j mice were randomly divided into the following four groups: Group A: normal control group (normal con); Group B: IAV control group (V con); Group C: IAV+ oseltamivir treatment group (V oseltamivir; 0.78 mg/mL, 0.2 mL/mouse/day); Group D: IAV+ forsythoside A treatment group (V FTA; 2 μg/mL, 0.2 mL/mouse/day). Real-time fluorescence quantitative PCR (RT-qPCR) was used to measure mRNA expression of the TLR7, MyD88, TRAF6, IRAK4 and NF-κB p65 mRNA in TLR7 signaling pathway and the virus replication level in lung. Western blot was used to measure TLR7, MyD88 and NF-κB p65 protein. Flow cytometry was used to detect the proportion of the T cell subsets Th1/Th2 and Th17/Treg. Results: The body weight began to decrease after IAV infection, while FTA and oseltamivir could reduce the rate of body weight loss. The pathological damages in the FTA and oseltamivir group were less serious. TLR7, MyD88, TRAF6, IRAK4 and NF-κB p65 mRNA were up-regulated after virus infection (p < 0.01) while down-regulated after oseltamivir and FTA treatment (p < 0.01). The results of TLR7, MyD88 and NF-κB p65 protein consisted with correlative mRNA. Flow cytometry showed the Th1/Th2 differentiated towards Th2, and the Th17/Treg cells differentiated towards Treg after FTA treatment. Conclusions: Our study suggests forsythoside A can control influenza A virus infection and improve the prognosis of IAV infection by inhibiting influenza A virus replication.
Highlights
Influenza infections represent a considerable public health burden
Based on the fact that the Toll-like receptor 7 (TLR7) signaling pathway is initially involved in microbial recognition by the2.1
Weight designed to test the hypothesis that Forsythoside A (FTA) could exert effects on the regulation of the TLR7 signaling
Summary
Influenza infections represent a considerable public health burden. Influenza viruses infect 3 to 5 million people worldwide [1,2]. Influenza illness is characterized by involvement of the respiratory tract accompanied by systemic complaints, including headache, myalgia, and fever [3]. A rapid immune response is required to control the lung infection. The role of innate immunity against influenza virus has been widely demonstrated to be essential of defense against viral infections through transmembrane cell receptors [4]. Toll-like receptor 7 (TLR7) is one of these receptors which can recognize viral single-stranded RNA (ssRNA) [5], activate the downstream signaling molecules through the MyD88-dependent pathway.
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