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慢性疲劳综合征患者外周血单个核细胞培养中细胞因子释放的改变。

Altered cytokine release in peripheral blood mononuclear cell cultures from patients with the chronic fatigue syndrome.

作者信息

Chao C C, Janoff E N, Hu S X, Thomas K, Gallagher M, Tsang M, Peterson P K

机构信息

Department of Medicine, Hennepin County Medical Center, Minneapolis, MN 55415.

出版信息

Cytokine. 1991 Jul;3(4):292-8. doi: 10.1016/1043-4666(91)90497-2.

Abstract

Chronic fatigue syndrome (CFS) is an idiopathic illness associated with a variety of immunologic abnormalities. To investigate potential pathogenetic mechanisms, we evaluated serum levels and peripheral blood mononuclear cell (PBMC) production of selected cytokines and immunoglobulins. Serum bioactive transforming growth factor beta (TGF-beta) levels were higher (P less than 0.01) in patients with CFS (290 +/- 46 pg/mL) than in control subjects (104 +/- 18 pg/mL), but levels of other cytokines tested were not different. Lipopolysaccharide-stimulated release of interleukin 1 beta (IL-1 beta), IL-6, and tumor necrosis factor-alpha was increased (P less than 0.05) in PBMC cultures from patients with CFS versus control subjects; enhanced (P less than 0.01) IL-6 release to phytohemagglutinin was also observed. In contrast, TGF-beta release in response to lipopolysaccharide was depressed (P less than 0.01) in PBMC cultures derived from patients with CFS. No differences in IL-2 and IL-4 or immunoglobulin production were observed. The enhanced release of inflammatory cytokines by stimulated PBMC from patients with CFS suggests that these cells are primed for an increased response to immune stimuli. These data also suggest an association between abnormal regulation of TGF-beta production in vivo and in vitro with the immunologic consequence of CFS.

摘要

慢性疲劳综合征(CFS)是一种与多种免疫异常相关的特发性疾病。为了研究潜在的发病机制,我们评估了血清水平以及外周血单个核细胞(PBMC)中特定细胞因子和免疫球蛋白的产生情况。CFS患者血清中生物活性转化生长因子β(TGF-β)水平(290±46 pg/mL)高于对照组(104±18 pg/mL)(P<0.01),但所检测的其他细胞因子水平并无差异。与对照组相比,CFS患者PBMC培养物中脂多糖刺激的白细胞介素1β(IL-1β)、IL-6和肿瘤坏死因子-α释放增加(P<0.05);还观察到对植物血凝素的IL-6释放增强(P<0.01)。相反,CFS患者来源的PBMC培养物中脂多糖刺激下的TGF-β释放受到抑制(P<0.01)。未观察到IL-2、IL-4或免疫球蛋白产生的差异。CFS患者受刺激的PBMC炎症细胞因子释放增强表明这些细胞对免疫刺激的反应增强。这些数据还表明体内和体外TGF-β产生的异常调节与CFS的免疫后果之间存在关联。

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