Schistosomiasis is listed as one of most important tropical diseases and more than 200 million people are estimated to be infected. Development of a vaccine is thought to be the most effective way to control this disease. Recombinant 26-kDa glutathione S-transferase (rSjGST) has previously been reported to achieve a worm reduction rate of 42–44%. To improve the efficiency of the vaccine against Schistosoma japonicum, we immunized mice with a combination of pcDNA vector-encoded 26-kDa SjGST (pcDNA/SjGST), IL-12 expressing-plasmid (pIL-12), and rSjGST. Co-vaccination with pcDNA/SjGST, pIL-12, and rSjGST led to a reduction in worm burden, hepatic egg burden, and the size of liver tissue granulomas than that in the untreated infection controls. In addition, we detected high levels of specific IgG, IgG1, and IgG2a against the rSjGST antigen in infected mice vaccinated with this combination of pcDNA/SjGST, pIL-12, and rSjGST. Moreover, high expression levels of Th2 cytokines, including IL-4 and IL-10, were also detected in this group, without diminished levels of IL-12, INF-γ, and TNF-α cytokines that are related to parasite killing. In conclusion, we have developed a new vaccination regimen against S. japonicum infection and shown that co-immunization with pcDNA/SjGST vaccine, pIL-12, and rSjGST has significant anti-parasite, anti-hepatic egg and anti-pathology effects in mice. The efficacy of this vaccination method should be further validated in large animals such as water buffalo. This method may help to reduce the transmission of zoonotic schistosomiasis japonica.
Inflammatory responses to microbial products are amplified by a pathway mediated by triggering a receptor expressed on the myeloid cells (TREM)-1. Relatively a few studies have been performed to investigate the role of TREM-1 in macrophage activation in response to parasitic infection. In this study, we delineate the role of the innate immunoreceptor TREM-1 in the parasite Schistosoma mansoni infection model from early to late (chronic) phases of infection. Flow cytometry analysis revealed gradual increase in the production of TREM-1 protein on CD11b(+) myeloid cells, with maximum production at 5 weeks p.i. Similar results in the pattern of TREM-1 mRNA expressions in splenic CD11b(+) cells from infected mice were obtained by real-time PCR. However, unlike in spleen, the TREM-1 mRNA expression in liver tissue showed no significant increase throughout the infection, including periods of maximum production of parasite eggs. Administration of schistosoma egg homogenate antigen to stimulate J774A.1 cells inhibited TREM-1 expression on the surface, indicating that some substances of the Schistosma eggs may inhibit the expression of TREM-1 on macrophages, lowering the macrophage-mediated inflammatory response of infected hosts.
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