Effect of IL-18 on intrauterine infection of HBV in mice on cell molecular level

IL-18 对小鼠宫内感染乙型肝炎病毒的细胞分子水平影响

阅读:1

Abstract

OBJECTIVE: The objective of this study is to investigate the effect of IL-18 on intrauterine infection of HBV (Hepatitis B Virus) in mice based on cellular and molecular level, and to analyze its mechanism, as well as the relationship between IL-18 and intrauterine infection of HBV. METHODS: Pregnant rats are taken as the study subjects and divided into two groups according to infection and non-infection, namely the study group and the control group. Firstly, the peripheral blood of rats and the blood of newborn mice are collected for the determination of hepatitis B in two-and-a-half pairs. Then, the levels of interleukin-18 (IL-18), interferon-γ (IFN-γ) and interleukin-4 (IL-4) in peripheral serum are detected by ELISA (Enzyme Linked Immunosorbent Assay). Finally, the two groups of horizontal values are compared and analyzed. The effect of IL-18 on intrauterine infection of HBV in mice is investigated based on the level of cell and molecular. RESULTS: The levels of IL-18, IFN-γ, IL-4 and IFN-γ/IL-4 in the two groups are compared and analyzed. The levels of IL-18, IFN-γ and IFN-γ/IL-4 in the study group are significantly lower than those in the control group, with statistical significance. However, the level of IL-4 in the study group is higher than that in the control group, with statistical significance. CONCLUSION: It is found that the decrease of HL-type specific response and the enhancement of Th2-type specific response in pregnant mice are closely related to HBV intrauterine infection. Moreover, the decrease of IL-18 secretion in peripheral blood may cause intrauterine infection of HBV. This study can make people better realize the mechanism of HBV intrauterine infection, and effectively help clinical prevention and treatment of intrauterine infection.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。