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首页> 外文期刊>Infection and immunity >Lipoarabinomannans derived from different strains of Mycobacterium tuberculosis differentially stimulate the activation of NF-kappa B and KBF1 in murine macrophages.
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Lipoarabinomannans derived from different strains of Mycobacterium tuberculosis differentially stimulate the activation of NF-kappa B and KBF1 in murine macrophages.

机译：来源于结核分枝杆菌不同菌株的脂寡糖甘露聚糖差异性地刺激了小鼠巨噬细胞中NF-κB和KBF1的活化。

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The inflammatory cytokine tumor necrosis factor alpha (TNF-alpha) is rapidly induced in macrophages after exposure to Mycobacterium tuberculosis. Recently it was shown that lipoarabinomannan (LAM) derived from an attenuated (H37Ra) strain of M. tuberculosis (AraLAM) was capable of macrophage activation and induction of TNF-alpha production, whereas LAM derived from the virulent Erdman strain (ManLAM) was considerably reduced in this activity. A critical component in the regulation of many genes central to immune function is the transcription factor NF-kappa B. Lipopolysaccharide (LPS)-mediated induction of TNF-alpha expression in murine macrophages has been demonstrated to be regulated in part by NF-kappa B. In this study, we demonstrate that AraLAM is capable of rapid activation of NF-kappa B- and KBF1-binding activities in C3H/HeN bone marrow-derived macrophages and the J774.A and RAW264.7 murine macrophagelike cell lines, whereas ManLAM is considerably less potent at stimulating NF-kappa B. Treatment of RAW264.7 cells with AraLAM or LPS results in the stimulation of DNA binding of both forms within 7.5 min, which peaks within 30 min and 1 h, respectively. Interestingly, treatment of RAW264.7 macrophage-like cells with AraLAM, LPS, or ManLAM for greater than 2 h resulted in significant accumulation of KBF1. Inhibition of protein synthesis blocked the transient nature of NF-kappa B activation as well as the accumulation of KBF1. Using Western immunodetection of the NF kappa B1 p50 subunit, we also show that AraLAM and LPS stimulate the loss of the NF kappa B1 p105 precursor. These results demonstrate that NF-kappa B and KBF1 are rapidly induced in response to AraLAM and may play a role in avirulent M. tuberculosis activation of TNF-alpha expression in macrophages. The differential temporal regulation of kappa B element DNA-binding activities and the transient stimulation of NF kappa B followed by the sustained accumulation of KBF1 may serve as a feedback switch ensuring transient induction of TNF-alpha transcription.
机译：暴露于结核分枝杆菌后，巨噬细胞中迅速诱导出炎性细胞因子肿瘤坏死因子α（TNF-alpha）。最近显示，来自结核分枝杆菌（AraLAM）减毒株（H37Ra）的脂阿拉伯糖甘露聚糖（LAM）能够巨噬细胞激活和诱导TNF-α的产生，而源自强毒Erdman株（ManLAM）的LAM却相当可观。减少这项活动。转录因子NF-κB是调节许多对免疫功能至关重要的基因的重要组成部分。脂多糖（LPS）介导的鼠巨噬细胞TNF-α表达的诱导已部分被NF-κB调节。在这项研究中，我们证明AraLAM能够在C3H / HeN骨髓巨噬细胞以及J774.A和RAW264.7鼠巨噬细胞样细胞系中快速激活NF-κB和KBF1结合活性。在刺激NF-κB方面的效力大大降低。用AraLAM或LPS处理RAW264.7细胞会在7.5分钟内刺激两种形式的DNA结合，分别在30分钟和1小时内达到峰值。有趣的是，用AraLAM，LPS或ManLAM处理RAW264.7巨噬细胞样细胞超过2小时会导致KBF1大量积聚。蛋白质合成的抑制作用阻止了NF-κB激活的短暂性以及KBF1的积累。使用Western免疫检测的NF kappa B1 p50亚基，我们还显示AraLAM和LPS刺激了NF kappa B1 p105前体的损失。这些结果表明，NF-κB和KBF1响应AraLAM被快速诱导，并且可能在巨噬细胞中无毒的结核分枝杆菌激活TNF-α表达中起作用。 κB元素DNA结合活性的时空差异调节和NFκB的瞬时刺激，随后KBF1的持续积累，可以作为确保瞬时诱导TNF-α转录的反馈开关。

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