TUMOR-NECROSIS-FACTOR-ALPHA PRODUCTION BY HUMAN FETAL MICROGLIAL CELLS - REGULATION BY OTHER CYTOKINES
TUMOR-NECROSIS-FACTOR-ALPHA PRODUCTION BY HUMAN FETAL MICROGLIAL CELLS - REGULATION BY OTHER CYTOKINES
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DOI：
10.1159/000111278
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发表时间：
1995-03-01
影响因子：
2.9
通讯作者：
PETERSON, PK
中科院分区：
文献类型：
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作者：
CHAO, CC;HU, SX;PETERSON, PK
肿瘤坏死因子（TNF）-α被认为在发育中的脑内发挥重要的生理和病理作用。在本研究中，我们发现人胎儿小胶质细胞在脂多糖（LPS）刺激后释放大量的TNF-α。用白细胞介素（IL）-6，IL-10和转化生长因子（TGF）-β特异性抗体处理小胶质细胞培养物可增强LPS刺激的TNF-α释放。这些细胞因子中的每一种都剂量依赖性地抑制TNF-α的释放。此外，TNF-α mRNA的表达被这些细胞因子中的每一种抑制。通过对比，用单独的IL-α或IL-1 β或在LPS存在下处理小胶质细胞培养物导致TNF-α的释放增加，并且IL-1刺激TNF-α mRNA的表达。这些发现表明，这些细胞因子可能会改变TNF-α在发育中的大脑中的有益和有害作用。
Tumor necrosis factor (TNF)-alpha has been postulated to play an important physiologic as well as pathologic role within the developing brain. In the present study, we found that human fetal microglial cells released abundant amounts of TNF-alpha upon stimulation with lipopolysaccharide (LPS). Treatment of microglial cell cultures with antibodies specific to interleukin (IL)-6, IL-10, and transforming growth factor (TGF)-beta augmented LPS-stimulated release of TNF-alpha. Each of these cytokines dose-dependently suppressed TNF-alpha release. Also, TNF-alpha mRNA expression was inhibited by each of these cytokines. By way of contrast, treatment of microglial cell cultures with IL-alpha or IL-1 beta alone or in the presence of LPS, resulted in increased release of TNF-alpha, and IL-1 stimulated the expression of TNF-alpha mRNA. These findings suggest that these cytokines are likely to modify the beneficial and harmful effects of TNF-alpha within the developing brain.