Endogenous glucocorticoid increases the basal level of Treg-Th17 balance under early phase of stress

Abstract

【Abstract】 Objective: To explore the changes of Treg-Th17 balance influenced by corticosterone, major ef-fect hormone of hypothalamic-pituitary-adrenal (HPA) axis under running stress. Methods: A total of 25 corticotropin-releasing hor-mone (CRH) wildtype (CRH+/+) and knockout (CRH-/-) mice were adopt and divided into 4 groups as follows: CRH+/+ ctrl, CRH+/+ stress, CRH-/- ctrl and CRH-/- stress. All mice in stress groups were under 2 h running. After 1 h, blood plasma in all groups was collected and the ex-pression of corticosterone and IL-17A was detected by ELISA. Meanwhile, unicell suspensions of peripheral lymph node and spleen in each group were prepared too and stained by PE-CD4 and FITC-CD25, then the changes of Treg (CD4+CD25+) in different groups were checked by flow cytometry; all data were statistically analyzed by the software of WinMDI 2.9, SPSS 11.5, Origin 7.5 and Matlab 2-D and 3-D plot function. Results: The levels of corticosterone were signifi-cantly higher in stress groups than that in correspond-ing control groups (P<0.05), especially in CRH+/+ stress group (P<0.01). However, the changes of Tregs were not obvious between stress groups and control groups with respective genotypes (P<0.05). Compared with that in CRH+/+ control group, the ratio of Treg and the expres-sion of IL-17A in CRH-/- stress group were significantly higher than those in control group (P<0.05). Combined with the expression levels of corticosterone, Treg and Th17, our study suggests that endogenous glucocorti-coid with basal level may cause the changes in Treg-Th17 balance. Moreover, as the corticosterone level increases, the expression of Treg and Th17 appears to manifest antagonistic fluctuant status with a rising ten-dency in general. Conclusion: Endogenous glucocorticoid under early stage of stress may increase the function of T lymphocyte immunity to some extent. Key words: Stress disorders, post-traumatic; Glucocorticoids; Corticotropin-releasing hormone