4.7 Article

Melatonin as Immune Potentiator for Enhancing Subunit Vaccine Efficacy against Bovine Viral Diarrhea Virus

期刊

VACCINES
卷 9, 期 9, 页码 -

出版社

MDPI
DOI: 10.3390/vaccines9091039

关键词

BVDV; melatonin; the NF-kappa B inflammation pathway; T-cell immunity

资金

  1. National key R&D Program of China [2017YFD0502200]
  2. Program for the Beijing Dairy Industry Innovation Team (Beijing, China)

向作者/读者索取更多资源

The study found that adding MT to the E-rns-LTB vaccine can reduce the phosphorylation of p65 protein caused by BVDV infection and affect some immune-related factors, showing its potential for inhibiting BVDV infection. In addition, in mice experiments, treatment with E-rns-LTB + MF59 + MT also achieved some success.
Bovine viral diarrhea virus (BVDV) is a pathogen associated with substantial economic losses in the dairy cattle industry. Currently, there are no effective vaccines against BVDV. Melatonin (MT) has been shown to have anti-inflammatory and anti-viral properties, and the use of MF59 in vaccines significantly enhances vaccine efficiency. Here, MT and MF59 were added into the E-rns-LTB vaccine. Subsequently, their inhibitory activity on the NF-kappa B signaling pathway in Mardin-Darby Bovine Kidney cells and the hippocampus was assessed using western blot and quantitative reverse transcription PCR. The findings revealed that MT in the E-rns-LTB vaccine decreases the phosphorylation of p65 proteins caused by BVDV infection. In addition, MT decreased the mRNA levels of IL-1 beta and IL-6 in vitro, but increased the production of IFN-alpha, IFN-beta, Mx1 in vitro, brain-derived neurotrophic factor, cyclic amp response element-binding protein, and the stem cell factor in vivo. Furthermore, treatment with E-rns-LTB + MF59 + MT stimulated the production of T lymphocytes, alleviated pathological damage, decreased expressions of BVDV antigen, and tight junction proteins in mice. These findings imply that MT has potential for use in the E-rns-LTB vaccine to inhibit BVDV infection and regulate the immune responses of T-cells by inhibiting the NF-kappa B signaling pathway.

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