Immunogenicity of adenovirus and DNA vaccines co-expressing P39 and lumazine synthase proteins of Brucella abortus in BALB/c mice.

Brucella poses a great threat to animal and human health. Vaccination is the most promising strategy in the effort to control Brucella abortus (B. abortus) infection, but the currently used live vaccines interfere with diagnostic tests and could potentially result in disease outbreak. Therefore, new subunit vaccines and combined immunization strategies are currently under investigation. In this study, immunogenicity and protection ability of a recombinant adenovirus and plasmid DNA vaccine co-expressing P39 and lumazine synthase proteins of B. abortus were evaluated based on the construction of the two molecular vaccines. Four immunization strategies (single adenovirus, single DNA, adenovirus/DNA, DNA/adenovirus) were investigated. The results showed that the immunization strategy of DNA priming followed by adenovirus boosting induced robust humoral and cellular immune responses, and it significantly reduced the numbers of B. abortus in a mouse model. These results suggest that it could be a potential antigen candidate for development of a new subunit vaccine against B. abortus infection.

ChREBP and LXRα mediate synergistically lipogenesis induced by glucose in porcine adipocytes.

Glucose is a substrate for fatty acid synthesis, and induces lipogenesis and expressions of lipogenic genes. It was proposed that transcriptional factor ChREBP, LXRα and SREBP-1c are key mediators in lipogenesis induced by glucose, however the underlying mechanism remains unclear in porcine adipocytes. In this study, glucose stimulated lipogenesis and expressions of ChREBP, LXRα, SREBP-1c and lipogenic genes FAS and ACC1 in primary porcine adipocytes. When ChREBP expression was knocked down by RNAi, lipogenesis and FAS and ACC1 expressions decreased significantly, and lipogenesis induced by glucose decreased by 75.6%, whereas neither the basal expressions under glucose-free nor glucose induced expressions of LXRα and SREBP-1c were evidently affected, suggesting that ChREBP was a main mediator of lipogenesis stimulated by glucose. Glucose promoted LXRα gene expression, and activation of LXRα by T0901317 increased SREBP-1c expression and enhanced the stimulation of glucose on lipogenesis, but this stimulatory effect of LXRα depended on glucose. Activated LXRα stimulated lipogenesis and ChREBP mRNA expression, which was much lower than that elevated by glucose, and was markedly lower in ChREBP-silencing than in unperturbed adipocytes. SREBP-1c activation blocked by fatostatin markedly decreased lipogenesis and expressions of FAS and ACC1 induced by glucose. Lipogenesis and lipogenic gene expression stimulated by LXRα activation were attenuated by fatostatin, however there was still a slightly increase in ChREBP-silencing adipocytes. These dates suggested that LXRα could directly or through SREBP-1c mediate the lipogenesis induced by glucose. Together, glucose induced lipogenesis and lipogenic gene expressions directly through ChREBP, and directly through LXRα or via SREBP-1c.