D3.159 - Investigation of Huai Qi Huang Granules' Impact and Mechanism on Asthmatic Mice's Antiviral Capability

Poster abstract

Background

Due to the unique characteristics of their immune systems, children with asthma are more susceptible to respiratory infections, with respiratory syncytial virus (RSV) infections being the most common. Huai Qi Huang Granules (HQHG) is an immunomodulator that helps strengthen immunity and increase a child's resistance to common infections. Research on employing immunomodulators to enhance the antiviral potential of children with asthma is currently lacking. The aim of this study is to generate a mouse model of asthma infected with RSV, evaluate the effect of HQHG on the animal's resistance to infection, and explore any plausible underlying processes.

Method

Six groups (normal control, group A, asthma model, group B, RSV infection, group C, asthma + RSV infection, group D, RSV infection + HQHG, group E, and asthma + RSV infection +HQHG,group F) were randomly assigned to thirty male Balb/c mice. Ovalbumin sensitization and challenge were used to cause asthma, and then an RSV nasal inoculation was administered. HQHG was administered to the mice. Important variables were tracked, including body weight, clinical symptoms, and survival rate. HE staining was used to examine lung tissue for pathological alterations and inflammatory cell infiltration. In lung tissue, qPCR measured the amount of virus, inflammatory variables, and genes linked to virus replication. The amounts of inflammatory factors in serum and lung tissue were evaluated using ELISA.

Results

Groups B, C, and D displayed greater death rates and more severe clinical symptoms (P<0.01) in comparison to Group A. Significant damage and infiltration of inflammatory cells were seen in lung tissue (P<0.01), accompanied by elevated viral load and viral protein expression (P<0.05). In addition, compared to Groups B and C, Group D showed greater serum levels of IL-4, IL-5, IL-6, TNF-α, and IFN-γ as well as increased inflammatory markers in lung tissue (P<0.001). Comparing Groups E and F to Groups B, C, and D, treatment with HQHG increased survival rates (P<0.05), considerably decreased symptom scores (P<0.01), lessened lung tissue damage (P<0.01), and reduced viral load and viral protein expression (P<0.05). Furthermore, Group F's serum levels of IL-4, IL-5, IL-6, TNF-α, and IFN-γ as well as lung tissue exhibited significantly lower levels of inflammatory markers than Group D (P<0.05).

Conclusion

In a mouse model of asthma, HQHG dramatically increases the antiviral ability as demonstrated by decreased viral load, attenuated inflammatory responses, reduced tissue damage, and improved clinical outcomes. Nevertheless, more research is required to determine the precise mechanisms underlying these effects in order to give a thorough theoretical framework for therapeutic application.

Topic