联合CovRS双组分调控系统与通过克林达米辛治疗的纳达酶诱导在Streptococcus pyogenes中
Ichiro Tatsuno1, Masanori Isaka1, Tadao Hasegawa1
1Department of Bacteriology, Nagoya City University Graduate School of Medical Sciences, Japan.
Japanese journal of infectious diseases
|March 31, 2024
概括
高剂量克林达米辛 (CLI) 治疗可以诱导Streptococcus pyogenes中的NAD-糖酶 (NADase). 该研究发现,CovS蛋白对于这种依赖克林达米辛的NADase诱导至关重要,独立于SpeB.
科学领域:
- 微生物学 微生物学
- 分子生物学分子生物学
- 毒理学 毒理学 毒理学
背景情况:
- 链球菌毒性休克综合征 (STSS) 用高剂量的克林达米辛 (CLI) 和青素治疗.
- 全球范围内正在出现抗CLI的Streptococcus pyogenes菌株.
- 在某些菌株中,CLI治疗可以增加NAD-糖酶 (NADase) 外毒素活性.
研究的目的:
- 为了研究在Streptococcus pyogenes中依赖CLI的NADase诱导背后的机制.
- 为了确定与这种现象有关的特定遗传因素.
主要方法:
- 使用了13种由CLI敏感性Streptococcus pyogenes1529菌株衍生而来的两组分传感器淘汰菌株.
- 在这些淘汰菌株中评估了依赖CLI的NADase诱导表型.
- 具体研究了CovS,SpeB,Maga和Rgg的作用.
主要成果:
- 对CLI敏感和对CLI耐药的Streptococcus pyogenes菌株表现出依赖于CLI的NADase诱导.
- 只有1529ΔcovS淘汰菌株失去了CLI-依赖的NADase诱导表型.
- 淘汰杆菌株1529ΔspeB,1529Δmga和1529Δrgg保留了该表型.
结论:
- 两组分传感器CovS对于在Streptococcus pyogenes中依赖于CLI的NADase诱导至关重要.
- 这种诱导途径的调节由CovS独立于SpeB进行.
- 了解这种机制可能会为针对CLI耐药菌株的策略提供信息.
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