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首页> 外文期刊>Cytokine >TNF-alpha is a potent inducer for IFN-inducible protein-10 in hepatocytes and unaffected by GM-CSF in vivo, in contrast to IL-1beta and IFN-gamma.
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TNF-alpha is a potent inducer for IFN-inducible protein-10 in hepatocytes and unaffected by GM-CSF in vivo, in contrast to IL-1beta and IFN-gamma.

机译：与IL-1beta和IFN-γ相比，TNF-α是肝细胞中IFN诱导型蛋白10的有效诱导剂，在体内不受GM-CSF的影响。

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摘要

We have recently shown that IFN-inducible protein 10 (IP-10), a member of the CXC chemokine family, is induced in hepatocytes surrounded by infiltrative mononuclear cells in human livers with chronic hepatitis. Hence, we examined the kinds of stimuli that can induce IP-10 expression in hepatocytes in vivo. While the liver expressed three chemokine genes (IP-10, JE/MCP-1, KC/GRO) in a tissue-specific fashion following systemic treatment with pro-inflammatory cytokines, IP-10 mRNA expression showed the most marked liver-specificity. Pretreatment with GM-CSF selectively inhibited IL-1beta, but not TNF-alpha-induced IP-10 mRNA expression. In situ hybridization analysis in the liver and Northern hybridization analysis in isolated liver cell fractions from rodents treated with pro-inflammatory cytokines revealed cellular sources of chemokine expression. IP-10 mRNA expression in hepatocytes was induced by i.v. administration of TNF-alpha, and to a much lesser extent in response to IL-1beta and IFN-gamma, whereas Kupffer cells and endothelial cells expressed IP-10 mRNA equivalently in response to these three stimuli. On the other hand, JE/MCP-1 mRNA expression was detected only in non-parenchymal cells in response to TNF-alpha and IL-1beta, but not in response to IFN-gamma. KC/GRO mRNA expression was also induced mainly in sinusoidal cells by treatment with TNF-alpha or IL-1beta, although it was detected to a lesser extent in hepatocytes. Our results demonstrated that chemokine induction is stimulus-, tissue- and cell type-specific and that IP-10 (but not MCP-1) is inducible in hepatocytes by TNF-alpha most potently, even in the presence of GM-CSF, suggesting the specific role of TNF-alpha-induced IP-10 on intralobular mononuclear infiltration in chronic hepatitis. Copyright 2000 Academic Press.
机译：我们最近显示，在慢性肝炎的人肝中，CXC趋化因子家族的成员IFN诱导蛋白10（IP-10）在被浸润性单核细胞包围的肝细胞中被诱导。因此，我们研究了在体内可诱导IP-10在肝细胞中表达的刺激物的种类。在使用促炎细胞因子进行全身治疗后，肝脏以组织特异性方式表达了三个趋化因子基因（IP-10，JE / MCP-1，KC / GRO），而IP-10 mRNA表达则显示出最明显的肝特异性。 GM-CSF预处理选择性抑制IL-1β，但不抑制TNF-α诱导的IP-10 mRNA表达。肝脏中的原位杂交分析和来自用促炎性细胞因子处理的啮齿动物的分离的肝细胞部分中的Northern杂交分析揭示了趋化因子表达的细胞来源。 i.v.诱导肝细胞IP-10 mRNA表达。 TNF-α的使用，对IL-1beta和IFN-γ的响应程度要小得多，而Kupffer细胞和内皮细胞在对这三种刺激的响应中均表达IP-10 mRNA。另一方面，仅在非实质细胞中检测到JE / MCP-1 mRNA表达，以响应TNF-α和IL-1beta，但未检测到IFN-γ。 KC / GRO mRNA表达也主要通过使用TNF-α或IL-1beta处理在正弦细胞中诱导，尽管在肝细胞中的表达程度较低。我们的结果表明，趋化因子诱导是刺激，组织和细胞类型特异性的，即使在存在GM-CSF的情况下，TNF-α也能最有效地诱导肝细胞中的IP-10（而非MCP-1）。 TNF-α诱导的IP-10在慢性肝炎小叶内单核浸润中的特定作用。版权所有2000学术出版社。

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