干扰素诱导鸟苷酸结合蛋白1可调节脂多糖诱导的细胞因子/凝血因子和巨噬细胞中的丝裂原活化蛋白激酶。

IF 1.9 4区 医学 Q4 IMMUNOLOGY
Ravindra Kumar, Pramod Kumar Kushawaha
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引用次数: 0

摘要

鸟苷酸结合蛋白(GBPs)是干扰素(IFN)诱导型 GTP 酶家族的一员,在宿主对微生物感染的免疫反应中发挥着关键作用。这些蛋白在识别革兰氏阴性细菌的主要膜成分脂多糖(LPS)后在免疫细胞中上调。本研究初步绘制了 GBP1-7 在 LPS 刺激下的表达模式图,这些细胞系分别是经磷酸果胶 12 肉豆蔻酸 13 醋酸酯分化的人单核细胞 THP-1 和小鼠巨噬细胞 RAW 264.7。在这些细胞中,GBP1-7 的表达具有时间依赖性。此外,在各种 GBPs 中,GBP1 已成为调节先天免疫和炎症的核心角色。因此,为了研究 GBP1 在 LPS 诱导的炎症中的特殊作用,我们使用小干扰 RNA 干扰技术在这两种细胞中敲除了 Gbp1 基因。与对照细胞相比,GBP1 基因敲除细胞中不同细胞因子(白细胞介素 [IL]-4、IL-10、IL-12β、IFN-γ、肿瘤坏死因子-α)、诱导型一氧化氮合酶、组织相容性 2、II 类抗原 A、蛋白激酶 R 和趋化因子(趋化因子(C-X-C motif)配体 9 [CXCL9]、CXCL10 和 CXCL11)的水平均有所改变。有趣的是,与对照细胞相比,敲除细胞中的细胞外信号调节激酶 1/2丝裂原活化蛋白(MAP)激酶和信号转导及激活转录因子 1(STAT1)转录因子的水平显著提高。然而,与对照细胞相比,GBP1敲除细胞中磷酸化核因子-kB、c-Jun和p38转录因子的水平没有变化。本研究的结论是,GBP1 可能会改变由 MAP 激酶和 STAT1 转录因子介导的细胞因子、趋化因子和效应分子的表达。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Interferon inducible guanylate-binding protein 1 modulates the lipopolysaccharide-induced cytokines/chemokines and mitogen-activated protein kinases in macrophages

Guanylate-binding proteins (GBPs) are a family of interferon (IFN)-inducible GTPases and play a pivotal role in the host immune response to microbial infections. These are upregulated in immune cells after recognizing the lipopolysaccharides (LPS), the major membrane component of Gram-negative bacteria. In the present study, the expression pattern of GBP1–7 was initially mapped in phorbol 12-myristate 13-acetate-differentiated human monocytes THP-1 and mouse macrophages RAW 264.7 cell lines stimulated with LPS. A time-dependent significant expression of GBP1–7 was observed in these cells. Moreover, among the various GBPs, GBP1 has emerged as a central player in regulating innate immunity and inflammation. Therefore, to study the specific role of GBP1 in LPS-induced inflammation, knockdown of the Gbp1 gene was carried out in both cells using small interfering RNA interference. Altered levels of different cytokines (interleukin [IL]-4, IL-10, IL-12β, IFN-γ, tumor necrosis factor-α), inducible nitric oxide synthase, histocompatibility 2, class II antigen A, protein kinase R, and chemokines (chemokine (C-X-C motif) ligand 9 [CXCL9], CXCL10, and CXCL11) in GBP1 knockdown cells were reported compared to control cells. Interestingly, the extracellular-signal-regulated kinase 1/2 mitogen-activated protein (MAP) kinases and signal transducer and activator of transcription 1 (STAT1) transcription factor levels were considerably induced in knockdown cells compared to the control cells. However, no change in the level of phosphorylated nuclear factor-kB, c-Jun, and p38 transcription factors was observed in GBP1 knockdown cells compared to the control cells. This study concludes that GBP1 may alter the expression of cytokines, chemokines, and effector molecules mediated by MAP kinases and STAT1 transcription factors.

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来源期刊
Microbiology and Immunology
Microbiology and Immunology 医学-免疫学
CiteScore
5.20
自引率
3.80%
发文量
78
审稿时长
1 months
期刊介绍: Microbiology and Immunology is published in association with Japanese Society for Bacteriology, Japanese Society for Virology, and Japanese Society for Host Defense Research. It is peer-reviewed publication that provides insight into the study of microbes and the host immune, biological and physiological responses. Fields covered by Microbiology and Immunology include:Bacteriology|Virology|Immunology|pathogenic infections in human, animals and plants|pathogenicity and virulence factors such as microbial toxins and cell-surface components|factors involved in host defense, inflammation, development of vaccines|antimicrobial agents and drug resistance of microbes|genomics and proteomics.
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