TY - JOUR
T1 - Repetitive restraint stress changes spleen immune cell subsets through glucocorticoid receptor or β-adrenergic receptor in a stage dependent manner
AU - Li, Yu
AU - Jiang, Wei
AU - Li, Zhen zhen
AU - Zhang, Chen
AU - Huang, Chen
AU - Yang, Jun
AU - Kong, Guang yao
AU - Li, Zong fang
N1 - Publisher Copyright:
© 2017 Elsevier Inc.
PY - 2018/1/1
Y1 - 2018/1/1
N2 - Immune system is sensitive to stress. Spleen is the largest peripheral immune organ innervated with sympathetic nerves and controlled by adrenomedullary system in the body. However, the alterations and mechanism of spleen immune cell subsets caused by repetitive restraint stress (RRS) is poorly understood. In this study, we found that RRS reduced spleen index in mice, and induced an expansion of white pulp and involution of the red pulp. Meanwhile, the percentage of CD3+CD8+ T lymphocytes, CD11b+F4/80+ macrophages, CD11b+Ly-6G−Ly-6Chi monocytic myeloid derived suppressor cells (mMDSCs) and CD11b+Ly-6G+Ly-6Cint granulocytic myeloid derived suppressor cells (gMDSCs) in spleen were significantly changed by RRS. Mechanistically, we found that the expression of norepinephrine (NE) and β-adrenergic receptor (β-AR) in spleen were up-regulated after 21 days of RRS, but not 7 days. The expression of corticosterone (CORT) and glucocorticoid receptor (GR) in spleen were up-regulated after 7 days of RRS but were lower after 21 days of RRS, even though they were still higher than that in mice without stress. By treating the stressed mice with RU486 (antagonist of GR) or propranolol (antagonist of β-AR), we demonstrated that GR was responsible for the changes of spleen induced by 7 days of RRS and β-AR was for 21 days of RRS. Our data suggest that RRS changes spleen immune cell subsets through GR or β-AR in a stage dependent manner.
AB - Immune system is sensitive to stress. Spleen is the largest peripheral immune organ innervated with sympathetic nerves and controlled by adrenomedullary system in the body. However, the alterations and mechanism of spleen immune cell subsets caused by repetitive restraint stress (RRS) is poorly understood. In this study, we found that RRS reduced spleen index in mice, and induced an expansion of white pulp and involution of the red pulp. Meanwhile, the percentage of CD3+CD8+ T lymphocytes, CD11b+F4/80+ macrophages, CD11b+Ly-6G−Ly-6Chi monocytic myeloid derived suppressor cells (mMDSCs) and CD11b+Ly-6G+Ly-6Cint granulocytic myeloid derived suppressor cells (gMDSCs) in spleen were significantly changed by RRS. Mechanistically, we found that the expression of norepinephrine (NE) and β-adrenergic receptor (β-AR) in spleen were up-regulated after 21 days of RRS, but not 7 days. The expression of corticosterone (CORT) and glucocorticoid receptor (GR) in spleen were up-regulated after 7 days of RRS but were lower after 21 days of RRS, even though they were still higher than that in mice without stress. By treating the stressed mice with RU486 (antagonist of GR) or propranolol (antagonist of β-AR), we demonstrated that GR was responsible for the changes of spleen induced by 7 days of RRS and β-AR was for 21 days of RRS. Our data suggest that RRS changes spleen immune cell subsets through GR or β-AR in a stage dependent manner.
KW - Glucocorticoid receptor
KW - Propranolol
KW - RU486
KW - Repetitive restraint stress
KW - Spleen
KW - β-adrenergic receptor
UR - https://www.scopus.com/pages/publications/85034831838
U2 - 10.1016/j.bbrc.2017.11.148
DO - 10.1016/j.bbrc.2017.11.148
M3 - 文章
C2 - 29175389
AN - SCOPUS:85034831838
SN - 0006-291X
VL - 495
SP - 1108
EP - 1114
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 1
ER -