title: Endogenous glucocorticoid increases the basal level of Treg-Th17 balance under early phase of stress.
abstract: OBJECTIVE
  To explore the changes of Treg-Th17 balance influenced by corticosterone, major effect hormone of hypothalamic-pituitary-adrenal (HPA) axis under running stress.
  
  
  METHODS
  A total of 25 corticotropin-releasing hormone (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 expression 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 significantly higher in stress groups than that in corresponding control groups (P less than 0.05), especially in CRH+/+ stress group (P less than 0.01). However, the changes of Tregs were not obvious between stress groups and control groups with respective genotypes (P less than 0.05). Compared with that in CRH+/+ control group, the ratio of Treg and the expression of IL-17A in CRH-/- stress group were significantly higher than those in control group (P less than 0.05). Combined with the expression levels of corticosterone, Treg and Th17, our study suggests that endogenous glucocorticoid 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 tendency in general.
  
  
  CONCLUSIONS
  Endogenous glucocorticoid under early stage of stress may increase the function of T lymphocyte immunity to some extent.
authors.affiliation: State Key Laboratory of Trauma, Burns and Combined Injury, Research Institute for Traffic Medicine, Department 4, Institute of Surgery Research/Daping Hospital, Third Military Medical University, Chongqing 400042, China.
authors.forename: Hai-yan
authors.initials: HY
authors.lastname: Wang
authors.forename: Wen-ting
authors.initials: WT
authors.lastname: Gao
authors.forename: Qing-hua
authors.initials: QH
authors.lastname: He
authors.forename: Ce
authors.initials: C
authors.lastname: Yang
authors.forename: Wei
authors.initials: W
authors.lastname: Gu
authors.forename: Jun
authors.initials: J
authors.lastname: Yan
authors.forename: Jian-xin
authors.initials: JX
authors.lastname: Jiang
mesh_terms: D000818:Animals; D015704:CD4 Antigens / Q000378:metabolism*; D003345:Corticosterone / Q000097:blood*; D003346:Corticotropin-Releasing Hormone / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D005434:Flow Cytometry; D020381:Interleukin-17 / Q000378:metabolism*; D053645:Interleukin-2 Receptor alpha Subunit / Q000378:metabolism*; D008198:Lymph Nodes / Q000166:cytology; D051379:Mice; D018345:Mice, Knockout; D010913:Pituitary-Adrenal System / Q000378:metabolism; D012420:Running / Q000502:physiology; D013154:Spleen / Q000166:cytology; D013312:Stress, Physiological; D058504:Th17 Cells / Q000378:metabolism*
chemical_list: D015704:CD4 Antigens; D020381:Interleukin-17; D053645:Interleukin-2 Receptor alpha Subunit; D003346:Corticotropin-Releasing Hormone; D003345:Corticosterone