Plain Language Summary
Thymosin alpha-1 combined with cyclosporine A shifted the immune balance in mice from pro-inflammatory Th1 toward anti-inflammatory Th2 responses, lowering IL-1-alpha, IL-2, IL-6, and IL-17 while raising IL-10. These results suggest thymosin alpha-1 has regulatory effects on immune signaling molecules that could be useful in managing transplant rejection or autoimmune conditions.
Abstract
OBJECTIVE: To analysis the effects of Talpha1 on the immune effector molecules in mouse immune system.
METHODS: Sixty five BABL/c mice were divided into four groups: CsA group (n=20), Talpha1 group (n= 20), CsA+Talpha1 group (n=20) and control group (n=5). In the 3 experimental groups, 10 mg/kg CsA, 400 microg/ kg Talpha1, 10 mg/kg CsA+400 microg/kg Talpha1 were respectively administrated by intraperitoneal injection daily. Luminex was performed for cytokine detection at 1 d, 7 d, 14 d, 21 d day after the above treatments. Lymphocyte culture was prepared with the mouse spleen suspension, and then treated with 0. 25 mg/mL CsA, 10 microg/mL Talpha1 or 0.25 mg/mL CsA+10 microg/mL Talpha1 in vitro, respectively. Three days later, OD values of each treated lymphocyte culture and several cytokines in the culture were measured.
RESULTS: Compared with other groups, CsA+Talpha1 group had significant lower IL-1alpha, IL-2, IL-6, IL-17, and significant higher IL-10 at 1 d, 7 d, 14 d, 21 d after the treatments (P < 0.05). Three days after the culture, OD value in the control group was significantly higher than that in Talppha1 group, CsA group, and CsA+ Talpha1 group (P < 0.05). IL-1alpa and IL-6 in the control group were significantly higher than those in the experiment groups (P < 0.05), while IL-10 in the control group was significantly lower than that in the experiment groups (P < 0.05). IL-2 and IL-17 were similar.
CONCLUSION: Talpha1 show regulatory effect on the immune effector molecules which could promote Th1 cells transforming to Th2 cells.
Authors
Li, Wei-ye; Lu, Hui-min; Guo, Qiang; Hu, Wei-ming; Zhang, Zhao-da