斯特雷普托利辛S以依赖离子流入的方式诱导促炎性细胞因子表达
Yugo Yamamori1, Rina Shirai1, Kazuto Ohkura2
1Division of Bioresource Science, Graduate School of Sciences and Technology for Innovation, Tokushima University Graduate School, 2-1 Minamijousanjima-cho, Tokushima, Tokushima 770-8513, Japan.
这种细菌是Streptococcus anginosus亚种. 痛症 (SAA) 分泌Streptolysin S (SLS),一种毒素,导致人体细胞中的流入和炎症. 这种机制有助于SAA在子宫外感染中的致病性.
科学领域:
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- 性小组链球菌 (AGS) 是口腔机会性病原体.
- 这是一种β-溶血型的Streptococcus anginosus亚种. 痛症 (SAA) 产生链球素S (SLS).
- AGS越来越多地与子宫外感染分离,需要进行病原性研究.
研究的目的:
- 阐明宿主细胞对从SAA.分泌的SLS的反应机制.
- 调查SLS在外阴感染中AGS致病性中的作用.
主要方法:
- 人类急性单细胞白血病THP-1细胞的化与含有SLS.的SAA培养超体.
- 测量Ca2+流入和促炎性细胞因子表达.
- 在Ca2+化条件下对细胞因子基因表达的分析.
- 对细胞外信号调节激酶 (ERK) 和p38基激活蛋白激酶 (MAPK) 途径的研究.
主要成果:
- 在THP-1细胞中,SLS诱导了增加的Ca2+流入和增加的前炎性细胞因子表达.
- 确定Ca2+流入是SLS依赖细胞反应的触发因素.
- 依赖于SLS的IL-8表达与ERK和p38 MAPK通路激活有关.
结论:
- 通过SLS介导的Ca2+流入和随后的炎症性细胞因子产生是SAA病原性的关键机制.
- 了解这些途径对于解决SAA在子宫外感染中的作用至关重要.
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