Social isolation stress exacerbates autoimmune disease in MRL/lpr mice
Social isolation stress exacerbates autoimmune disease in MRL/lpr mice
复制标题
DOI：
10.1016/j.jneuroim.2004.09.002
复制
发表时间：
2005-01-01
影响因子：
3.3
通讯作者：
Kubo, C
中科院分区：
文献类型：
--
作者：
Chida, Y;Sudo, N;Kubo, C
解释心理社会压力对自身免疫性疾病影响的潜在生理机制尚未确定。暴露于慢性社会隔离应激的MRL/lpr小鼠20周龄后蛋白尿的程度显着增加，并降低生存率。血清抗双链DNA IgG 2a水平显着增加应力在19周龄，这是同时伴随着抑制血清皮质酮升高。此外，应激导致抗CD 3刺激的脾单核细胞产生IFN-λ增加，而IL-4和IL-10产生减少。这些结果表明，隔离应激加重了MRL/lpr小鼠自身免疫性疾病，其机制可能与应激诱导Th 1/Th 2平衡失调和抑制血皮质酮对炎症刺激的反应有关。由爱思唯尔公司出版
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-lambda 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. Published by Elsevier B.V.