金霉素 A53 的促炎特性。

IF 2.6 4区 医学 Q3 IMMUNOLOGY
Justyna Śmiałek-Bartyzel , Monika Bzowska , Paweł Mak
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引用次数: 0

摘要

Aureocin A53 是由机会性病原体金黄色葡萄球菌菌株 A53 产生的一种多肽细菌素。与氨基酸序列不同,金黄色葡萄球菌素的空间结构与细菌素 BacSp222 相似,后者最近被发现具有诱导宿主细胞产生炎症反应的能力。本研究旨在验证金黄色葡萄球菌素 A53 也具有这种特性。我们证明,合成的金黄色葡萄球菌素对小鼠单核-巨噬细胞细胞有轻微的细胞毒性。该分子还能激活小鼠 P388.D1 和 RAW 264.7 细胞产生 IFN-γ 依赖性一氧化氮,并激活促炎细胞因子 TNF 的产生。我们还证明,所观察到的细菌素的促炎活性与刺激 TLR2/TLR6 异二聚体有关,从而激活了 NF-κB 转录因子。总之,A53 是文献中描述的第二种对小鼠巨噬细胞样细胞具有促炎活性的细菌素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pro-inflammatory properties of aureocin A53

Aureocin A53 is a peptide bacteriocin produced by an opportunistic pathogen Staphylococcus aureus strain A53. The spatial structure of aureocin, unlike its amino acid sequence, is similar to the bacteriocin BacSp222, which was recently found to have the ability to induce the inflammatory response in the host cells. The presented research aimed to verify such properties also for aureocin A53. We demonstrated that the synthetic aureocin has slight cytotoxic activity towards murine monocytic-macrophage cells. This molecule was also able to activate murine P388.D1 and RAW 264.7 cells to IFN-γ-dependent production of nitric oxide and to activate production of the pro-inflammatory cytokine - TNF. We also proved that the observed pro-inflammatory activity of the studied bacteriocin is related to the stimulation of the TLR2/TLR6 heterodimer and, consequently, activation of the NF-κB transcription factor. To sum up, A53 is the second bacteriocin described in the literature, showing the pro-inflammatory activity against murine macrophage-like cells.

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来源期刊
Microbes and Infection
Microbes and Infection 医学-病毒学
CiteScore
12.60
自引率
1.70%
发文量
90
审稿时长
40 days
期刊介绍: Microbes and Infection publishes 10 peer-reviewed issues per year in all fields of infection and immunity, covering the different levels of host-microbe interactions, and in particular: the molecular biology and cell biology of the crosstalk between hosts (human and model organisms) and microbes (viruses, bacteria, parasites and fungi), including molecular virulence and evasion mechanisms. the immune response to infection, including pathogenesis and host susceptibility. emerging human infectious diseases. systems immunology. molecular epidemiology/genetics of host pathogen interactions. microbiota and host "interactions". vaccine development, including novel strategies and adjuvants. Clinical studies, accounts of clinical trials and biomarker studies in infectious diseases are within the scope of the journal. Microbes and Infection publishes articles on human pathogens or pathogens of model systems. However, articles on other microbes can be published if they contribute to our understanding of basic mechanisms of host-pathogen interactions. Purely descriptive and preliminary studies are discouraged.
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