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TGFβ1 induces IL-6 and inhibits IL-8 release in human bronchial epithelial cells: the role of Smad2/3.TGFβ1 诱导人支气管上皮细胞释放 IL-6 并抑制 IL-8 的释放:Smad2/3 的作用。
J Cell Physiol. 2010 Nov;225(3):846-54. doi: 10.1002/jcp.22295.
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NF-κB as a central regulator of macrophage function in tumors.NF-κB 作为肿瘤中巨噬细胞功能的中央调控因子。
J Leukoc Biol. 2010 Nov;88(5):877-84. doi: 10.1189/jlb.0310153. Epub 2010 Jun 23.
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Alternative activation of macrophages: mechanism and functions.巨噬细胞的替代激活:机制与功能。
Immunity. 2010 May 28;32(5):593-604. doi: 10.1016/j.immuni.2010.05.007.
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Epithelium: the interplay between innate and Th2 immunity.上皮组织:固有免疫与 Th2 免疫的相互作用。
Immunol Cell Biol. 2010 Mar-Apr;88(3):257-68. doi: 10.1038/icb.2009.113. Epub 2010 Jan 12.
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Early growth response transcription factors and the modulation of immune response: implications towards autoimmunity.早期生长反应转录因子与免疫应答的调节:对自身免疫的影响。
Autoimmun Rev. 2010 Apr;9(6):454-8. doi: 10.1016/j.autrev.2009.12.006. Epub 2009 Dec 23.
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The resolution of inflammation: anti-inflammatory roles for NF-kappaB.炎症的解决:NF-κB 的抗炎作用。
Int J Biochem Cell Biol. 2010 Apr;42(4):519-23. doi: 10.1016/j.biocel.2009.12.016. Epub 2009 Dec 22.
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The nuclear signaling of NF-kappaB: current knowledge, new insights, and future perspectives.NF-κB 的核信号转导:当前知识、新见解和未来展望。
Cell Res. 2010 Jan;20(1):24-33. doi: 10.1038/cr.2009.137. Epub 2009 Dec 8.
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Myeloid cells control termination of lung inflammation through the NF-kappaB pathway.髓样细胞通过NF-κB信号通路控制肺部炎症的消退。
Am J Physiol Lung Cell Mol Physiol. 2009 Mar;296(3):L320-7. doi: 10.1152/ajplung.90485.2008. Epub 2008 Dec 19.
9
Pulmonary epithelium is a prominent source of proteinase-activated receptor-1-inducible CCL2 in pulmonary fibrosis.肺上皮是肺纤维化中蛋白酶激活受体-1诱导的CCL2的主要来源。
Am J Respir Crit Care Med. 2009 Mar 1;179(5):414-25. doi: 10.1164/rccm.200712-1827OC. Epub 2008 Dec 5.
10
NF-kappaB mediates the survival of human bronchial epithelial cells exposed to cigarette smoke extract.核因子-κB介导暴露于香烟烟雾提取物的人支气管上皮细胞的存活。
Respir Res. 2008 Sep 23;9(1):66. doi: 10.1186/1465-9921-9-66.

上皮细胞调节与 NF-κB 激活相关的基因在共培养的人巨噬细胞中。

Epithelial cells modulate genes associated with NF kappa B activation in co-cultured human macrophages.

机构信息

Institute for Clinical and Experimental Medicine, Prague, Czech Republic.

出版信息

Immunobiology. 2011 Oct;216(10):1110-6. doi: 10.1016/j.imbio.2011.04.009. Epub 2011 May 1.

DOI:10.1016/j.imbio.2011.04.009
PMID:21601940
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4706171/
Abstract

Macrophages located in airways and the alveolar space are continually exposed to different signals from the respiratory mucosa. In this respect, epithelial cells represent an important source of cytokines and mediators modulating the state of activation and/or differentiation of mononuclear phagocytes. Many of the proinflammatory genes induced in macrophages during immune and immunopathological reactions are regulated by transcription factor NF kappa B. The aim of our study was to characterize changes in the expression of genes associated with NF kappa B activation and signalling in THP-1 human macrophages co-cultured with A549 respiratory epithelial cells. At least 4-fold upregulation of mRNA level was found in 29 of 84 tested genes including genes for multiple cytokines and chemokines, membrane antigens and receptors, and molecules associated with NF kappa B signalling. The mRNA induction was confirmed at the level of protein expression by evaluating the release of IL-6 and IL-8 and by ICAM-1 expression. Blocking of one NFκB subunit by p65 siRNA inhibited the production of IL-6 in both cell types while IL-8 release from THP-1 cells did not seem to be affected. We conclude from our data that unstimulated respiratory epithelial cells regulate genes associated with NF kappa B dependent immune responses in human macrophages and that these interactions may play a key role in immediate responses in the respiratory mucosa.

摘要

位于气道和肺泡空间的巨噬细胞不断受到来自呼吸道黏膜的不同信号的影响。在这方面,上皮细胞是调节单核吞噬细胞激活和/或分化状态的细胞因子和介质的重要来源。在免疫和免疫病理反应中,巨噬细胞中诱导的许多促炎基因受转录因子 NF-κB 调节。我们的研究目的是描述与 NF-κB 激活和信号转导相关的基因在与 A549 呼吸上皮细胞共培养的 THP-1 人巨噬细胞中的表达变化。在 84 个测试基因中,有 29 个基因的 mRNA 水平至少上调了 4 倍,包括多种细胞因子和趋化因子、膜抗原和受体以及与 NF-κB 信号转导相关的分子。通过评估 IL-6 和 IL-8 的释放以及 ICAM-1 表达,在蛋白质表达水平上证实了 mRNA 诱导。用 p65 siRNA 阻断一个 NFκB 亚基抑制了两种细胞类型中 IL-6 的产生,而 THP-1 细胞中 IL-8 的释放似乎不受影响。我们从数据中得出结论,未刺激的呼吸上皮细胞调节与人类巨噬细胞中 NF-κB 依赖性免疫反应相关的基因,这些相互作用可能在呼吸道黏膜的即刻反应中发挥关键作用。