内质网应激上调了神经胶质细胞中前列腺素E₂/γ干扰素诱导的白细胞介素-6表达，并下调了诱导型一氧化氮合酶的表达。
ER stress upregulated PGE₂/IFNγ-induced IL-6 expression and down-regulated iNOS expression in glial cells.
作者信息
Hosoi Toru, Honda Miya, Oba Tatsuya, Ozawa Koichiro
机构信息
Department of Pharmacotherapy, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan.
出版信息
Sci Rep. 2013 Dec 2;3:3388. doi: 10.1038/srep03388.
The disruption of endoplasmic reticulum (ER) function can lead to neurodegenerative disorders, in which inflammation has also been implicated. We investigated the possible correlation between ER stress and immune function using glial cells. We demonstrated that ER stress synergistically enhanced prostaglandin (PG) E₂ + interferon (IFN) γ-induced interleukin (IL)-6 production. This effect was mediated through cAMP. Immune-activated glial cells produced inducible nitric oxide synthase (iNOS). Interestingly, ER stress inhibited PGE₂ + IFNγ-induced iNOS expression. Similar results were obtained when cells were treated with dbcAMP + IFNγ. Thus, cAMP has a dual effect on immune reactions; cAMP up-regulated IL-6 expression, but down-regulated iNOS expression under ER stress. Therefore, our results suggest a link between ER stress and immune reactions in neurodegenerative diseases.
内质网（ER）功能紊乱可导致神经退行性疾病，炎症也与这些疾病有关。我们使用神经胶质细胞研究了内质网应激与免疫功能之间的可能关联。我们证明内质网应激协同增强了前列腺素（PG）E₂ + 干扰素（IFN）γ诱导的白细胞介素（IL）-6生成。这种效应是通过环磷酸腺苷（cAMP）介导的。免疫激活的神经胶质细胞产生诱导型一氧化氮合酶（iNOS）。有趣的是，内质网应激抑制了PGE₂ + IFNγ诱导的iNOS表达。当用二丁酰环磷腺苷钙（dbcAMP）+ IFNγ处理细胞时也获得了类似结果。因此，cAMP对免疫反应具有双重作用；在应激状态下，cAMP上调IL-6表达，但下调iNOS表达。因此，我们的结果提示了神经退行性疾病中内质网应激与免疫反应之间的联系。
Zotero 插件