The Study On IL-23/Th17 Axis In Chronic Sustained Model Of Experimental Autoimmune Encephalomyelitis

Objective To investigate the changes of IL-23p19, IL-17, IL-6mRNA expression in brains of induced chronic non-remitting model ofexperimental autoimmune encephalomyelitis (EAE), and discuss themechanism of IL-23/Th17cells axis on EAE/MS.Methods 72 adult female C57BL/6 mice were randomly dividedinto the adjuvant -control group, EAE groups, TGF-β1 treatmentgroups, treatment-control groups. MOG35-55 and CFA were injected intosubcutaneous in EAE groups. Animals in TGF-β1 treatment groupsreceived TGF-β1 subcutaneous injection. In addition to immunization,PBS was injected subcutaneously in the treatment-control groups. At theonset, peak and chronic post-immunization, the group mice weresacrificed. The expression of IL-23p19, IL-17, IL-6 mRNA in brainwere detected by using RT-PCR..Results 83.3% mice in EAE groups were developed aprogressive paralysis, which peaked at 20-24 days, and then exhibited achronic disease with a partial clinical recovery. In contrast, 88.9% micein TGF-β1 treatment groups developed the ealier progressive paralysis,which peaked at 17-22 days, and were more prone to recovery. There wereno remarkable difference between EAE and treatment-control groups.The expression of IL-23p19 mRNA of brains in EAE groups increased at early, followed by a descent in the peak phase and chronicphase(p＜0.05) In TGF-β1 treatment groups, The expression ofIL-23p19 mRNA in each phase dramatically deceased (p＜0.05) incontrast to the EAE groups.The expression of IL-17 mRNA of brains in EAE groupsincreased at the peak phase, while the expression of IL-17 mRNA inTGF-β1 increased dramaticly in the TGF-β1 treatment groups(p＜0.05).There was statistically difference in the expression of IL-6 betweenthe EAE group and the TGF-β1 treatment group(p＜0.05).The differencebetween the different phase in the same group was not prominent(p＞0.05)Conclusion1. The expression of IL-17 was correlated with the severity ofdisease,while the expression of IL-23p19 may play an important role inthe initiation of disease.2. Exogenous TGF-β1 may suppress the expression of IL-23p19and promote the expression of IL-17.3. IL-6 may play an important role in the different phase of EAE.