Premium
Cortisol is associated with low frequency of interleukin 10–producing B cells in patients with atherosclerosis
Author(s) -
Huo Yizhong,
Chu Yan,
Guo Lixin,
Liu Linli,
Xia Xiaojun,
Wang Tierui
Publication year - 2017
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.3262
Subject(s) - immune system , pathogenesis , inflammation , coronary atherosclerosis , medicine , endocrinology , cytokine , peripheral , b cell , interleukin , interleukin 6 , cell , immunology , biology , antibody , coronary artery disease , genetics
It is accepted that inflammation plays a critical role in the development of atherosclerosis; the pathogenesis is not clear. B‐cell–produced interleukin (IL) 10 is an immune regulatory cytokine that can inhibit immune inflammation. This study tests a hypothesis that a psychological stress hormone, cortisol, suppresses IL‐10 expression in peripheral B cells of patients with atherosclerosis. Peripheral blood samples were collected from patients with coronary artery atherosclerosis. B cells were isolated from the blood samples to be analyzed for the expression of IL‐10 and micro RNA (miR) 98 by real‐time polymerase chain reaction. We observed that the frequency of IL‐10 + B cell was less in patients with atherosclerosis than healthy controls. The serum cortisol levels were higher in the patients than that in healthy controls. Peripheral B‐cell frequency was negatively correlated with the serum cortisol levels. Exposure of B cells to cortisol increased the expression of miR‐98 in B cells. Cortisol also inhibited the expression of IL‐10 in B cells, in which miR‐98 played a critical role. Treating B cells from atherosclerosis patients with anti–miR‐98 liposomes reversed the ability of expression of IL‐10 in the cells. The expression of IL‐10 is suppressed in peripheral B cells, which can be up regulated by anti–miR‐98 liposomes.