| Summary: | 【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
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