OBJECTIVETo investigate whether allitridin could interfere with the effects of murine cytomegalovirus (MCMV) infection on the transcription, expression and function of IL-12 genes in order to further explore the mechanism of allitridin against MCMV.

METHODSixty mice were randomly divided into allitridin treated group, placebo and blank controls. Allitridin was intra-peritoneal injected to mice in treated group once a day with general dosage (25 mg x kg(-1)) at 24 hours after MCMV infection, and the same dosage of physiological saline were given to placebo and blank groups. Four experimental mice were sacrificed at 3, 5, 7, 10, 14 days after treatment (n = 4 per time point), respectively. The expression of IL-12 p70 and IFN-gamma in supernatant of spleen cell cultures were measured by double-antibody sandwich ELISA, and IL-12 p35 and p40 mRNAs in spleen cells were analyzed by RT-PCR.

RESULTIn systemic infection mice, the expression of both IL-12 p70 protein and p35 mRNA significantly increased on day 3 post-infection (pi); then rapidly and markedly decreased on day 5 pi and later. The level of IFN-gamma reached the peak on day 3 pi, then gradually dropped and returned to normal levels during the period of day 10 to 14 pi, and IL-12 p40 mRNA level was persistently and significantly higher after infection. In allitridin treated mice, the levels of IL-12 p70 protein, IL-12 p35 and p40 mRNAs reached the peak on day 3 after treatment (P < 0.05), and then rapidly dropped to the normal levels during the period of 5-14 days. Level of IFN-gamma was also reached the peak on day 3 after treatment; however, it dropped a little on day 5 and then gradually increased and was much higher than those of both placebo and bland controls during the period of day 7 to 14 after treatment (P < 0.01).

CONCLUSIONAllitridin could completely correct the disturbance of expression of IL-12 gene caused by MCMV and persistently promote IFN-gamma expression, which was useful for enhancing the specific cellular immune reactions against CMV and clearance of CMV viruses from host. The result suggests another mechanism of allitridin against CMV.