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斯特雷普托利辛S诱导明显的离子流入依赖的表达直接早期的编码转录因子的基因表达

Takuya Yamada¹, Yugo Yamamori², Nanami Matsuda²

¹Department of Biological Science and Technology, Life System, Institute of Technology and Science, Tokushima University Graduate School, 2-1 Minamijousanjima-Cho, Tokushima, Tokushima, 770-8506, Japan.

Scientific reports

|August 22, 2023

概括

性 estreptococcus secretes streptolysin S (SLS),一种毒素,增加流入和基因表达口腔细胞. 这一发现有助于理解这些机会性病原体的致病性.

科学领域:

口腔微生物学口腔微生物学
细菌病原体的发生.
细胞毒性的分子机制

背景情况:

性小组链球菌 (AGS) 是机会性口腔病原体.
这是Streptococcus anginosus亚种的β-溶血子组. 痛症产生Streptolysin S (SLS),这是一个细胞毒性血解素.
精确的SLS细胞毒性和宿主细胞反应机制尚不清楚.

研究的目的:

为了研究产生SLS的β血解性S. anginosus亚种的致病潜力. 痛性. 痛性. 这种情况很常见.
为了阐明人类口腔状细胞癌HSC-2细胞中依赖于SLS的细胞反应.

主要方法:

化HSC-2细胞与培养SLS产生的β-血溶性S. anginosus亚种的超体. 痛性. 痛性. 这种情况很常见.
测量Ca2+的流入.
立即早期基因表达 (IEG) 的分析,包括早期生长反应 (EGR) 和激活蛋白-1 (AP-1).
评估Ca2+化对基因表达的影响.

主要成果:

生产SLS的S. anginosus亚种. 痛症在HSC-2细胞中显著增加了Ca2+的流入.
包括EGR和AP-1在内的IEGs的表达明显增强.
2+化抑制了依赖于SLS的IEG表达的增加,除了jun.
这些发现表明SLS诱导Ca2+流入,导致IEG转录因子表达的增强.

结论:

来自β血解性S. anginosus亚种的SLS. 痛会触发Ca2+的流入,并随后对即时早期基因的上调调节.
了解这些分子事件对于阐明SLS产生AGS的病原性至关重要.
这项研究提供了关于涉及口腔链球菌的宿主-病原体相互作用的见解.

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