The Effects of Allitridin on the Expression of Transcription Factor T-bet／GATA-3 in Mice Infected by Murine Cytomegalovirus

Objective: To investigate the effects of allitridin on the expression of transcription factor T-bet/GATA-3 in mice infected by murine cytomegalovirus. Methods: 20 BALB/c mice were randomly divided into allitridin treated group(n = 10) and placebo controls group( n = 10). Allitridin therapy group were given to mice via the intraperitoneal (i. p.) route once a day with general dosage (25mg/kg) at 24 hours after infected MCMV; placebo controls group were given with the same volume of 0.89% sodium chloride. Blank controls group (n = 10), the same volume of 0.89% sodium chloride was injected. All experimental mice were sacrificed at 14 days i. p. The spleens were removed under aseptic conditions, and infectious virus was quantified by plaque assay. The expression levels of transcription factor T-bet/GATA-3 were measured by RT-PCR. The expression levels of IFN-γ and IL-10 in supernatant of spleen cell culture were measured by ELISA. Results MCMV infection markedly down-modulated the expression of IFN-γ and T-bet mRNA, significantly up-modulated the expression of IL-10 and GATA-3 mRNA. Allitridin induced an increased expression of transcription factor T-bet mRNA and IFN-γ significantly (P < 0.01), decreased expression of transcription factor GATA-3 mRNA and IL-10 markedly (P < 0.01). MCMV-infected mice treated with allitridin showed a significant (P < 0.01) reduction in virus titers in the spleens compared to the untreated MCMV-infected mice. Conclusion: MCMV infection can lead to disequilibrium of TH1/ TH2 cytokine expression: the level of IFN-γ was significantly decreased and IL-10 overexpressed. Allitridin up-regulate the expression of T-bet mRNA and IFN-γ, and inhibit the expression of GATA-3 mRNA and IL-10 in MCMV infected mice, indicating a TH1 dominant state which will enhance the specific cellular immune reactions against cytomegalovirus and be helpful for clearance of cytomegalovirus in host.