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首页> 外文期刊>Infection and immunity >Salmonella Flagellin Induces Tumor Necrosis Factor Alpha in a Human Promonocytic Cell Line
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Salmonella Flagellin Induces Tumor Necrosis Factor Alpha in a Human Promonocytic Cell Line

机译：沙门氏菌鞭毛蛋白诱导人类单核细胞系中的肿瘤坏死因子α。

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During infection of the gastrointestinal tract, salmonellae induce cytokine production and inflammatory responses which are believed to mediate tissue damage in the host. In a previous study, we reported that salmonellae possess the ability to stimulate tumor necrosis factor alpha (TNF-α) accumulation in primary human monocytes, as well as in the human promonocytic cell line U38. In this model system, cytokine upregulation is not due to lipopolysaccharide but is mediated by a released protein. In the present study, TnphoA transposon mutagenesis was used to identify the TNF-α-inducing factor. A mutantSalmonella strain which lacks the ability to induce TNF-α was isolated from a TnphoA library. Genetic analysis of this mutant demonstrated that the hns gene has been interrupted by transposon insertion. The hns gene product is a DNA-binding protein that regulates the expression of a variety of unrelated genes in salmonellae. One of the known targets of histone-like protein H1 is flhDC, the master operon which is absolutely required for flagellar expression. Analysis of other nonflagellated mutant Salmonella strains revealed a correlation between the ability to induce TNF-α and the expression of the phase 1 filament subunit protein FliC. Complementation experiments demonstrated that FliC is sufficient to restore the ability of nonflagellated mutant Salmonella strains to upregulate TNF-α, whereas the phase 2 protein FljB appears to complement to a lesser extent. In addition, Salmonella FliC can confer the TNF-α-inducing phenotype on Escherichia coli, which otherwise lacks the activity. Furthermore, assembly of FliC into complete flagellar structures may not be required for induction of TNF-α.
机译：在胃肠道感染期间，沙门氏菌诱导细胞因子的产生和炎症反应，据信可介导宿主的组织损伤。在先前的研究中，我们报道了沙门氏菌具有刺激肿瘤坏死因子α（TNF-α）在原代人单核细胞以及人单核细胞系U38中积累的能力。在该模型系统中，细胞因子上调不是由于脂多糖引起的，而是由释放的蛋白质介导的。在本研究中，Tn phoA 转座子诱变用于鉴定TNF-α诱导因子。从Tn phoA 文库中分离出缺乏诱导TNF-α能力的突变株 Salmonella 。该突变体的遗传分析表明， hns 基因已被转座子插入所打断。 hns 基因产物是一种DNA结合蛋白，可调节沙门氏菌中各种无关基因的表达。组蛋白样蛋白H1的已知靶标之一是 flhDC ，这是鞭毛表达所必需的主操纵子。分析其他无鞭毛突变体 Salmonella 菌株后，发现诱导TNF-α的能力与1期细丝亚基蛋白FliC的表达之间存在相关性。补充实验表明，FliC足以恢复非鞭毛突变沙门氏菌菌株上调TNF-α的能力，而2期蛋白FljB似乎互补程度较低。此外，沙门氏菌 FliC可以赋予大肠杆菌TNF-α诱导表型，否则缺乏活性。此外，可能不需要将FliC组装成完整的鞭毛结构来诱导TNF-α。

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