Host MiR181a Regulates Immune Response Studies After Schistosomiasis Infection

Schistosomiasis japonica is a parasitic zoonosis caused by the infection of schistosoma japonicum.Praziquantel is currently the only drug which can effectively work on the mass treatment of Schistosomiasis.While it still cannot prevent one from repeated infection.We aim to consolidate prevention of schistosomiasis.Thus a promising vaccine that can effectively work and cause no harm is investigated.The key to schistosomiasis vaccine is the immunologic mechanism of schistosoma infection.In the previous research,mi R-181 a played an important role in the immune response of shcistosoma infection in the early stage.In this study,we primarily analysis the regulating role of mi R181 a in the early infection of schistosoma Japonicum,in Vivo and in Vitro.Firstly,q PCR was conducted to get the expression of mi R-181 a from different host(suitable host BALB/c mouse and non-permissive host M.fortis).We compare the mi R-181 a expression in host serum and liver in 0d,3d,7d,10 d,24d,32 d,42d post infection.The results show two different trend in mi R233 expression.The mi R181 a expression in mouse showed an upper trend after infection.While the mi R181 a expression in M.fortis showed an opposite trend.In conclusion,the different expression of mi R-181 a in host animals may regulate the growth and differentiation processes of schistosoma in host body.Experimental schistosomiasis infection are analyzed us ing different hosts in different times after mi R181 a expression of the situation,the study found that in the suitability of the host mice serum mi R 181 a increased expression and in the suitability of host vole east mi R181 a expression quantity.Then extracts two host liver cells for testing result is also in the suitability of the host mice serum mi R181 a increased expression and in the suitability of host vole east mi R181 a expression quantity.The study indicated that the expression difference of mi R181 a in the body of schistosomiasis infection was different in vivo,and that the expression difference of mi R181 a may be related to the immunity mechanism of Oriental voles.In order to further investigate the role of mi R181 a in host immune regulation during schistosoma japonicum infection,we used LPS to stimulate RAW264.7 macrophages.And q PCR indicated that increased the expression of fluorescent quantitative detection m TLR4 and mi R181 a expression quantity cut;LPS stimulated RAW264.7 macrophages,and transfec ted mi R181 a analogue and inhibitor.The expression level of proinflammatory cytokines IL-1β,IL-6,and TNF-α was up-regulated Using TL4 flaws in mice with the TL4 mice in vivo experiments,schistosomiasis TL4 flaws with the defect after rat found TL4 increased the expression of rat mi R181 a and non TL4 defects increased mi R181 a expression in mice.The results indicate that the mi R181 a may effect the expression of cytokines though affecting the TLR4 receptor pathwayThe results of this study provide valuable experimental evidence for elucidating the immunomodulatory effects of mi R181 a on Schistosoma japonicum infection and the mechanism of resistance against schistosomiasis in Oriental voles.