Abstract

BackgroundCystic echinococcosis (CE) is a parasitic disease that is caused by Echinococcus granulosus (Eg). The recombinant Echinococcus granulosus antigen P29 (rEg.P29) was shown to confer effective immunity to sheep and mice during E. granulosus secondary infection in our previous study. In this study, we sought to investigate the ability of long noncoding RNA 028466 (lncRNA028466) as a regulator for the protective immunity mediated by rEg.P29 vaccination and to study the effects of lncRNA028466 on CD4+T cell differentiation in mice spleen.MethodsFemale BALB/c mice were divided into two groups and were vaccinated subcutaneously with rEg.P29 antigen and PBS as a control (12 mice each group). Following prime-boost vaccination, CD4+T, CD8+T, and B cells from the spleen were isolated by flow cytometry. Quantitative real-time PCR (qRT-PCR) was performed to measure the expression of lncRNA028466 in these three kinds of cells. Then, lncRNA028466 was overexpressed and knocked down in naive CD4+T cells, and Th1 and Th2 cytokine expression was detected. qRT-PCR, western blot, and ELISA were performed to evaluate the production of IFN-γ, IL-2, IL-4, and IL-10, and flow cytometry was performed to detect the differentiation of Th1 and Th2 subgroups.ResultslncRNA028466 was significantly decreased after the second week of immunization with rEg.P29 antigen. The proportion of CD4+ T cells was increased after rEg.P29 immunization. Overexpression of lncRNA028466 facilitated the production of IL-4, IL-10 and suppressed the production of IFN-γ, IL-2. Furthermore, after transfection with siRNA028466, IL-2 production was facilitated and IL-10 production was suppressed in naive CD4+ T cells.ConclusionsImmunization with rEg.P29 downregulated the expression of lncRNA028466, which was related to a higher Th1 immune response and a lower Th2 immune response. Our results suggest that lncRNA028466 may be involved in rEg.P29-mediated immune response by regulating cytokine expression of Th1 and Th2.

Highlights

  • Cystic echinococcosis (CE) is a parasitic disease that is caused by Echinococcus granulosus (Eg)

  • Microarray analysis revealed that lncRNA028466 was immunization, Quantitative real-time PCR (qRT-PCR) was used to determine the downregulation of lncRNA028466. lncRNA028466 exhibited 1.87-fold-lower expression (t = 7.906, P = 0.0002) compared with that in the control group (Fig. 1b)

  • Because lncRNA028466 expression decreased in spleen lymphocytes of mice immunized with rEg.P29 antigen, we aimed to understand the role that lncRNA028466 played in rEg.P29-mediated immune response

Read more

Summary

Introduction

Cystic echinococcosis (CE) is a parasitic disease that is caused by Echinococcus granulosus (Eg). The recombinant Echinococcus granulosus antigen P29 (rEg.P29) was shown to confer effective immunity to sheep and mice during E. granulosus secondary infection in our previous study. Cystic echinococcosis (CE), known as hydatid disease, is a worldwide chronic parasitic disease, threatening the health of livestock and humans [1]. Humans are exposed to the eggs of Echinococcus granulosus after close contact with infected livestock or contaminated food [2, 3]. Due to the limitations of current diagnostic and therapeutic measures, numerous studies have been carried out in the field of immunology associated with E. granulosus infection in the hope of developing vaccines [6, 7]. Due to the complicated host-parasite relationship [9], there is still no commercial vaccine

Objectives
Methods
Results
Discussion
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.