Yan Weiping,Qin Xinyue,Huang Qi,Cheng Chuang.Effect of IL-27 on CCL5 expression in experimental autoimmune encephalomyelitis mice[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(13):1408-1412.
Yan Weiping,Qin Xinyue,Huang Qi,Cheng Chuang.Effect of IL-27 on CCL5 expression in experimental autoimmune encephalomyelitis mice[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(13):1408-1412.DOI:
Effect of IL-27 on CCL5 expression in experimental autoimmune encephalomyelitis mice
Objective To determine regulating effect of interleukin-27 (IL-27) on the expression of central nervous system (CNS) chemokine RANTES (CCL5)
and investigate its therapeutic effect on experimental autoimmune encephalomyelitis (EAE) in mice. Methods EAE models were established in 40 female C57BL/6 mice by inoculating homogenate containing myelin oligodendrocyte glycoprotein (MOG
31-55
) and complete Freund’s adjuvant (CFA)
and then the rabbits wer
e killed in 0
7
14 and 21 d later for the expression of IL-27 and CCL5 in the CNS by Western blotting. Another 50 female C57BL/6 mice were randomly divided into normal control group
EAE group
EAE+IL-27 group
EAE+SC144 (IL-12 receptor inhibitor) group and EAE+PBS group. The behavior changes were observed. The expression of CCL5 at protein and mRNA levels was detected in the CNS by Western blotting and real-time PCR in 21 d after EAE model establishment. Results After EAE model was established
the expression of IL-27 in the CNS was increased with time elapse
while the expression of CCL5 was reduced with time. IL-27 intervention resulted in milder injury in neural function (
P
0.05)
while SC144 treatment enhanced the injury (
P
0.05). In 21 d after EAE model establishment
the mRNA and protein expression of CCL5 was significantly decreased in the IL-27 intervention group than the EAE model group (
P
0.05)
while the expression was increased significantly in SC144 group (
P
0.05). Conclusion In EAE mice
IL-27 suppresses the expression of CCL5 at protein and mRNA levels
and thus exerts an anti-inflammatory effect to reduce the nerve function
which might provide a new drug target for CNS autoimmune inflammatory disease.