Abstract:The protective effect and mechanism of Schistosoma japonicum cathepsin B (Sjcb2) DNA vaccine in the mouse model of schistosomiasis were studied through construction pcDNA3.1 (+) / Sjcb2 DNA recombinant vector, which provided effective candidate antigen for anti-schistosome vaccine. The 6-week-old female BALB/c mice were randomly divided into pcDNA3.1(+)/Sjcb2 DNA vaccine group, pcDNA3.1(+) plasmid group and normal saline group, respectively. Each group was composed of 35 mice, and 100 μg of Sjcb2 plasmid DNA was injected in the hind leg quadriceps of mice once every two weeks. PCR and immunohistochemistry assay were used to detect the expression and stability of Sjcb2 gene in mice. MTT assay was used for testing the specific proliferation response of mice spleen lymphocytes. The level of Sjcb2 antibodies in mouse serum and the IFN-γ and IL-4 levels in mice spleen lymphocyte culture supernatant before and after schistosome infection were assayed by ELISA. At last, we counted load of Schistosome adult worms in mouse and eggs in liver of mouse. The results showed that the Sjcb2 gene was detected in all mice of the Sjcb2 DNA vaccine group, and Sjcb2 gene expression was positive in the muscle cells in Sjcb2 DNA immunized mice by IHC assay. MTT assay showed that T-cell proliferation rate was increased significantly in Sjcb2 DNA vaccinated group. ELISA results showed that the IFN-γ levels were increased significantly in the vaccinated group, while the IL-4 levels were significantly increased after Schistosoma japonicum infection in all mice of every group. The load of worms and eggs in Sjcb2 DNA vaccinated group was reduced significantly than that of control group (P<0.05), the reduction rates of adult worms and eggs were 36.32% and 60.61% respectively. In conclusion, the Sjcb2 gene was stably expressed in muscle cells of mice after injection of Sjcb2 recombinant plasmid, and Sjcb2 produced protective effects of anti-schistosoma infection in mice possibly by mean of regulating Th1 cell subgroups through increasing the IFN-γ level and decreasing IL-4 levels.
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