Induction of lipopolysaccharide-binding protein gene expression in cultured rat pulmonary artery smooth muscle cells by interleukin 1 beta.

Induction of lipopolysaccharide-binding protein gene expression in cultured rat pulmonary artery smooth muscle cells by interleukin 1 beta.
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白细胞介素1β诱导培养的大鼠肺动脉平滑肌细胞中脂多糖结合蛋白基因的表达。

DOI:
10.1165/ajrcmb.12.4.7695925
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发表时间:
1995
期刊:
American journal of respiratory cell and molecular biology.
影响因子:
--
通讯作者:
Wang,SC
Wang,SC
中科院分区:
--
文献类型:
--
作者:
Wong,HR;Pitt,BR;Su,GL;Rossignol,DP;Steve,AR;Billiar,TR;Wang,SC

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脂多糖结合蛋白(LBP)与内毒素具有高亲和力,LBP-内毒素复合体可增强细胞对内毒素的炎症反应。虽然LBP存在于正常血清中,但LBP也是急性时相反应的一部分。虽然LBP的合成仅限于肝脏,但我们最近报道了在脓毒症和炎症的活体大鼠模型中肝外(包括肺)LBP mRNA的显著表达。在本研究中,我们通过将培养的大鼠肺动脉平滑肌细胞(RPASMC)暴露于细胞因子和内毒素,验证了大鼠肺LBP的细胞来源可能是血管平滑肌的假设。联合应用肿瘤坏死因子α、白介素1β(IL-1β)、干扰素-γ和脂多糖处理RPASMC 4和24 h后,LBP mRNA表达显著增加。在这种混合物中,单独的IL-1β足以以时间和剂量依赖的方式诱导LBP mRNA的表达。IL-1受体拮抗剂蛋白可明显拮抗IL-β对LBP基因表达的影响。此外,经IL-1β处理的RPASMC上清液可增强巨噬细胞系RAW 264.7与[125I]ASD-内毒素的结合,表明LBP具有生物活性。我们的结论是,在体外,IL-1β刺激的肺动脉平滑肌细胞产生LBP的转录本或同源产物。局部产生的LBP可能在肺部对炎症和脓毒症的反应中起重要作用。
Lipopolysaccharide (LPS)-binding protein (LBP) binds with high affinity to LPS, and the LBP-LPS complex enhances cellular inflammatory responses to LPS. Although it is present in normal serum, LBP is also induced as part of the acute phase response. Synthesis of LBP is though to be limited to the liver, but we have recently reported significant extrahepatic (including pulmonary) LBP mRNA expression in in vivo rat models of sepsis and inflammation. In the present study, we tested the hypothesis that a cellular source of pulmonary LBP in the rat may be vascular smooth muscle, by exposing cultured rat pulmonary artery smooth muscle cells (RPASMC) to cytokines and LPS. Treatment of RPASMC for 4 and 24 h with a combination of tumor necrosis factor alpha, interleukin 1 beta (IL-1 beta), interferon gamma, and LPS resulted in significant LBP mRNA expression. Of this mixture, IL-1 beta alone was sufficient to induce LBP mRNA expression in both a time- and dose-dependent manner. The effects of IL-beta on LBP mRNA expression were significantly antagonized by IL-1 receptor antagonist protein. Furthermore, supernatants from RPASMC treated with IL-1 beta enhanced the binding of [125I]ASD-LPS by the macrophage cell line RAW 264.7, indicative of LBP bioactivity. We conclude that pulmonary artery smooth muscle cells stimulated with IL-1 beta produce a transcript for LBP or a homologous product in vitro. Local production of LBP could play an important role in the pulmonary response to inflammation and sepsis.
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细菌脂多糖刺激巨噬细胞的新模型。
DOI: --
发表时间: 1990
期刊: The Journal of trauma
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