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首页> 外文期刊>Naunyn-Schmiedeberg's Archives of Pharmacology >Intravenous immunoglobulin preparation attenuates LPS-induced production of pro-inflammatory cytokines in human monocytic cells by modulating TLR4-mediated signaling pathways
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Intravenous immunoglobulin preparation attenuates LPS-induced production of pro-inflammatory cytokines in human monocytic cells by modulating TLR4-mediated signaling pathways

机译：静脉注射免疫球蛋白制剂可通过调节TLR4介导的信号通路减弱LPS诱导的人单核细胞促炎细胞因子的产生

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摘要

Intravenous immunoglobulin (IVIG) has been used for the treatment of inflammatory and autoimmune diseases. The ability to modulate cytokine production has been formerly described as one of the mechanisms of its action. This study aimed to investigate the effect of IVIG on the production of pro-inflammatory cytokines in lipopolysaccharide (LPS)-stimulated monocytic cells. Peripheral blood mononuclear cells (PBMCs) or THP-1 cells treated with phorbol myristate acetate (PMA) were stimulated with LPS. The protein levels of pro-inflammatory cytokines [tumor necrosis factor (TNF)-α, interleukin (IL)-6, and high-mobility group box 1 (HMGB1)] in the culture supernatants were determined using appropriate enzyme-linked immunosorbent assay kits. The mRNA of TNF-α was determined by reverse transcription–polymerase chain reaction. The phosphorylation of nuclear factor kappa B (NF-κB) and the mitogen-activated protein kinases was examined by Western blot analyses. IVIG suppressed the production of pro-inflammatory cytokines such as TNF-α and IL-6 in LPS-stimulated PBMCs. Furthermore, IVIG inhibited TNF-α, IL-6, and HMGB1 production from LPS-stimulated THP-1 cells treated with PMA. In addition, Fc fragment prepared from the IVIG inhibited production of these cytokines from the cells to the same degree as IVIG, whereas Fab and F(ab')2 fragments inhibited this only partially. We showed that IVIG and Fc fragments suppressed LPS-induced signal transduction pathways involving phosphorylation of NF-κB, p38, and c-Jun N-terminal kinase (JNK). Taken together, our results suggest that IVIG attenuates LPS-induced cytokine production predominantly mediated by its Fc region. The activity might be regulated by inhibiting NF-κB, p38, and JNK pathways in human monocytic cells.
机译：静脉内免疫球蛋白（IVIG）已用于治疗炎症和自身免疫性疾病。以前已经描述了调节细胞因子产生的能力是其作用机制之一。这项研究旨在调查IVIG对脂多糖（LPS）刺激的单核细胞中促炎性细胞因子产生的影响。用LPS刺激用佛波肉豆蔻酸酯乙酸盐（PMA）处理的外周血单核细胞（PBMC）或THP-1细胞。使用适当的酶联免疫吸附测定试剂盒测定培养上清液中促炎细胞因子的蛋白水平[肿瘤坏死因子（TNF）-α，白介素（IL）-6和高迁移率族框1（HMGB1）] 。 TNF-α的mRNA通过逆转录聚合酶链反应确定。通过蛋白质印迹分析检查核因子κB（NF-κB）和有丝分裂原激活的蛋白激酶的磷酸化。 IVIG抑制了LPS刺激的PBMC中促炎性细胞因子（如TNF-α和IL-6）的产生。此外，IVIG抑制了用PMA处理的LPS刺激的THP-1细胞产生的TNF-α，IL-6和HMGB1。此外，由IVIG制备的Fc片段以与IVIG相同的程度抑制了细胞中这些细胞因子的产生，而Fab和F（ab'）2 片段仅部分地抑制了这种产生。我们显示IVIG和Fc片段抑制LPS诱导的信号转导途径，涉及NF-κB，p38和c-Jun N末端激酶（JNK）的磷酸化。两者合计，我们的结果表明IVIG减弱主要由其Fc区介导的LPS诱导的细胞因子产生。可能通过抑制人单核细胞中的NF-κB，p38和JNK途径来调节活性。

著录项

  • 来源
    《Naunyn-Schmiedeberg's Archives of Pharmacology》 |2012年第9期|p.891-898|共8页
  • 作者

    Kazuki Murakami; Chiaki Suzuki; Fujio Kobayashi; Atsushi Nakano; Akihiro Fujii; Kaoru Sakai; Teruaki Imada;

  • 作者单位

    Research and Developmental Division, Benesis Corporation, 3-16-89, Kashima, Yodogawa-ku, Osaka-shi, Osaka, 532-8505, Japan;

    Research and Developmental Division, Benesis Corporation, 3-16-89, Kashima, Yodogawa-ku, Osaka-shi, Osaka, 532-8505, Japan;

    Research and Developmental Division, Benesis Corporation, 3-16-89, Kashima, Yodogawa-ku, Osaka-shi, Osaka, 532-8505, Japan;

    Research and Developmental Division, Benesis Corporation, 3-16-89, Kashima, Yodogawa-ku, Osaka-shi, Osaka, 532-8505, Japan;

    Research and Developmental Division, Benesis Corporation, 3-16-89, Kashima, Yodogawa-ku, Osaka-shi, Osaka, 532-8505, Japan;

    Research and Developmental Division, Benesis Corporation, 3-16-89, Kashima, Yodogawa-ku, Osaka-shi, Osaka, 532-8505, Japan;

    Research and Developmental Division, Benesis Corporation, 3-16-89, Kashima, Yodogawa-ku, Osaka-shi, Osaka, 532-8505, Japan;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    Intravenous immunoglobulin; LPS; Macrophages; TNF-α; NF-κB;

    机译：静脉注射免疫球蛋白;LPS;巨噬细胞;TNF-α;NF-κB;

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