Role of regulatory T cells in pathogenesis of heat stroke in rats

  Background  Heat stroke is characterized by high mortality and the cytological mechanism of the inflammatory response has not been elucidated.

  Objective  To investigate the changes of Tregs and related factors in serum and spleen after heat stroke (HS) in rats.

  Methods  Sixty adult male SD rats were randomly divided into control group (n=10) and HS group (n=50). Then HS group was divided into 5 subgroups (n=10) according to the sampling time points of 6 h, 12 h, 24 h, 48 h and 72 h after onset. The HS rat model was established in HS group. The serum cytokines TNF-α, IL-2, IL-6, TGF-β and IL-10 were detected. The percentage of Tregs in peripheral blood, spleen and the apoptosis rate of Tregs in spleen were detected by flow cytometry.

  Results  Compared with the control group, the serum cytokine levels in the HS group increased significantly at each time point (P＜0.05). The pro-inflammatory factors TNF-α and IL-2 peaked at 12 h and IL-6 peaked at 24 h. The anti-inflammatory factors TGF-β and IL-10 showed a gradually increasing trend. The proportion of Tregs in the serum of HS group was lower than that of the control group at 6 h (P＜0.05), and then gradually increased, while it was higher than that of the control group at 48 h and 72 h (P＜0.01). The proportion of Tregs in the spleen of the HS group was lower than that of the control group at 6 h and 12 h (P＜0.05), and then gradually increased, which was higher than that of the control group at 24 h, 48 h and 72 h. At 6 h, the apoptosis rate of Treg in the spleen of the HS group was higher than that of the control group, and then gradually decreased, which was lower than that of the control group at 24 h (P＜0.05). Pearson correlation analysis showed that the changes in IL-10 and TGF-β in serum were positively correlated with the changes in Tregs of blood and spleen and negatively correlated with the apoptosis rate of Tregs in spleen tissue.

  Conclusion  Tregs are probably involved in the pathogenesis of HS by regulating the changes of inflammatory factors IL-10 and TGF-β.