The effects of allitridin on the expression of transcription factors T-bet and GATA-3 in mice infected by murine cytomegalovirus.
This study was designed to investigate the effects of allitridin on the expression of transcription factors T-bet and GATA-3 in mice infected by murine cytomegalovirus (MCMV). A BALB/c mouse model system of MCMV infection was established. Twenty mice were allocated randomly into an allitridin-treated group (n = 10) and a placebo control group (n = 10). The same dose (25 mg/kg/day) and regimen of allitridin were used in the treated group in the 24 hours after virus infection; the same volume of saline solution was injected in placebo control mice. In an additional blank control group (n = 10), the same volume of saline solution was injected. The expression levels of the transcription factors T-bet and GATA-3 were measured by reverse transcription-polymerase chain reaction. The expression levels of the T helper (Th) 1 cytokine interferon-gamma (IFN-gamma) and the Th2 cytokine interleukin (IL)-10 in supernatant of spleen cell culture were measured by enzyme-linked immunosorbent assay. MCMV infection markedly down-modulated the expression of IFN-gamma and T-bet and significantly up-modulated the expression of IL-10 and GATA-3. Allitridin induced significantly (P < .01) increased expression of the transcription factor T-bet and the Th1 cytokine IFN-gamma and markedly (P < .01) decreased expression of the transcription factor GATA-3 and the Th2 cytokine IL-10. Thus MCMV infection could lead to disequilibrium of Th1/Th2 cytokine expression: The level of the Th1 cytokine IFN-gamma was decreased significantly, and Th2 cytokine IL-10 was overexpressed markedly. Allitridin could up-regulate the expression of T-bet and IFN-gamma and inhibit the expression of GATA-3 and IL-10 in MCMV-infected mice, indicating a Th1 dominant state, which should enhance the specific cellular immune reactions against cytomegalovirus (CMV) and be helpful for clearance of CMV from the host.
Yi
Xu
X
The Laboratory of Pediatric Clinical Virology of Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. xuyi70@163.com
Feng
Fang
F
Xiang
Zhidan
Z
Ge
Li
L
D000498:Allyl Compounds / Q000494:pharmacology*; D000818:Animals; D004268:DNA-Binding Proteins / Q000235:genetics*; D050990:GATA3 Transcription Factor; D005737:Garlic; D015870:Gene Expression / Q000187:drug effects*; D006566:Herpesviridae Infections / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D018146:Muromegalovirus; D013440:Sulfides / Q000494:pharmacology*; D020825:T-Box Domain Proteins; D015534:Trans-Activators / Q000235:genetics*; D014157:Transcription Factors / Q000235:genetics*; D000098815:T-bet Transcription Factor
D000498:Allyl Compounds; D004268:DNA-Binding Proteins; D050990:GATA3 Transcription Factor; C494748:Gata3 protein, mouse; D013440:Sulfides; D020825:T-Box Domain Proteins; D000098815:T-bet Transcription Factor; D015534:Trans-Activators; D014157:Transcription Factors; C042577:diallyl trisulfide