TY - JOUR
T1 - Social isolation stress exacerbates autoimmune disease in MRL/lpr mice
AU - Chida, Yoichi
AU - Sudo, Nobuyuki
AU - Kubo, Chiharu
N1 - Funding Information:
This study was supported by grants in aid for General Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology, Japan (No. 15659160 and No. 16390200).
PY - 2005/1
Y1 - 2005/1
N2 - The potential physiological mechanisms explaining an influence of psychosocial stress on autoimmune diseases remain undetermined. Exposure of chronic social isolation stress to MRL/lpr mice significantly enhanced the degree of proteinuria after 20 weeks of age and reduced the survival rate. The serum anti-dsDNA IgG2a levels were increased significantly by stress at 19 weeks of age, which was simultaneously accompanied by inhibition of the serum corticosterone elevation. Furthermore, stress caused increased IFN-γ production from anti-CD3-stimulated splenic mononuclear cells, whereas IL-4 and IL-10 production decreased. These results indicated that isolation stress exacerbated autoimmune disease in MRL/lpr mice, the possible mechanism for which might be related to stress-induced dysregulation of Th1/Th2 balance and inhibition of the blood corticosterone response to inflammatory stimuli.
AB - The potential physiological mechanisms explaining an influence of psychosocial stress on autoimmune diseases remain undetermined. Exposure of chronic social isolation stress to MRL/lpr mice significantly enhanced the degree of proteinuria after 20 weeks of age and reduced the survival rate. The serum anti-dsDNA IgG2a levels were increased significantly by stress at 19 weeks of age, which was simultaneously accompanied by inhibition of the serum corticosterone elevation. Furthermore, stress caused increased IFN-γ production from anti-CD3-stimulated splenic mononuclear cells, whereas IL-4 and IL-10 production decreased. These results indicated that isolation stress exacerbated autoimmune disease in MRL/lpr mice, the possible mechanism for which might be related to stress-induced dysregulation of Th1/Th2 balance and inhibition of the blood corticosterone response to inflammatory stimuli.
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U2 - 10.1016/j.jneuroim.2004.09.002
DO - 10.1016/j.jneuroim.2004.09.002
M3 - Article
C2 - 15589047
AN - SCOPUS:10344259637
SN - 0165-5728
VL - 158
SP - 138
EP - 144
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
IS - 1-2
ER -