ALTERED CYTOKINE RELEASE IN PERIPHERAL-BLOOD MONONUCLEAR CELL-CULTURES FROM PATIENTS WITH THE CHRONIC FATIGUE SYNDROME

被引:153
作者
CHAO, CC
JANOFF, EN
HU, SX
THOMAS, K
GALLAGHER, M
TSANG, M
PETERSON, PK
机构
[1] HENNEPIN CTY MED CTR, DEPT MED, MINNEAPOLIS, MN 55415 USA
[2] UNIV MISSISSIPPI, MED CTR, SCH MED, DEPT MED, JACKSON, MS 39216 USA
[3] R&D SYST INC, MINNEAPOLIS, MN 55413 USA
[4] VET ADM MED CTR, DEPT MED, MINNEAPOLIS, MN 55417 USA
关键词
D O I
10.1016/1043-4666(91)90497-2
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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-β) levels were high (P < 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 1β (IL-1β), IL-6, and tumor necrosis factor-alpha was increased (P < 0.05) in PBMC cultures from patients with CFS versus control subjects; enhanced (P < 0.01) IL-6 release to phytohemagglutinin was also observed. In contrast, TGF-β release in response to lipopolysaccharide was depressed (P < 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-β production in vivo and in vitro with the immunologic consequence of CFS. © 1991.
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页码:292 / 298
页数:7
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