专门的细菌雌激酶可以逆转脂多糖的无处不在,以阻止免疫传感
Magdalena Szczesna1, Yizhou Huang1, Rachel E Lacoursiere2
1Department of Infectious Disease, Centre for Bacteriology Resistance Biology, Imperial College London, London, SW7 2AZ, UK.
像Burkholderia这样的致病细菌使用TssM来逆转LPS上的无处不在,逃避宿主细胞免疫力. 这种细菌雌激酶活性是毒性和颠覆抗菌自的关键.
科学领域:
- 细胞和分子微生物学
- 细菌病原体的产生
- 宿主-病原体相互作用
背景情况:
- 细胞自主免疫保护宿主细胞免受细菌感染.
- 环指蛋白213 (RNF213) 标志着细胞质中的细菌通过脂聚糖 (LPS) 的无处不在来破坏.
- 目前尚不清楚细胞醇适应的病原体是否在LPS上无处不在,并逃脱RNF213免疫力.
研究的目的:
- 为了研究细菌双化酶 (DUBs) 是否可以逆转LPS无处不在.
- 确定这种机制是否被病原体用来逃避宿主细胞自主免疫.
- 阐明细菌TssM雌激酶活性的结构基础和毒性作用.
主要方法:
- 生物化学试验以表征LPS上的TssM雌激酶活性.
- 在没有TssM的情况下,细菌遗传学评估RNF213依赖的无处不在.
- 结构生物学来确定TssM雌激酶功能的机制.
- 在体外和基于细胞的测试来研究细菌复制和自逃避.
主要成果:
- 伯克霍尔迪亚二维基酶TssM作为一种强大的酶,直接逆转LPS无处不在.
- 在没有TssM的情况下,细胞质Burkholderia被RNF213无处不在,并被自所准.
- TssM表达使沙门氏菌能够在细胞质中复制,而Burkholderia则采用多层防御,包括阻断自.
- 结构分析揭示了TssM的未合的雌激酶活性,在其他病原体中作为毒性因子保留.
结论:
- 细菌TssM利用酶活性逆转RNF213介导的LPS无处不在,这是一种逃避宿主细胞自主免疫力的新机制.
- 这种细菌毒性策略允许像Burkholderia这样的病原体在宿主细胞细胞溶液内繁殖.
- TssM同类体代表了一种保存的细菌机制,通过准LPS无处不在来破坏宿主防御.
更多相关视频
05:31Purification and Visualization of Lipopolysaccharide from Gram-negative Bacteria by Hot Aqueous-phenol Extraction
Published on: May 28, 2012
10:24Separation of the Cell Envelope for Gram-negative Bacteria into Inner and Outer Membrane Fractions with Technical Adjustments for Acinetobacter baumannii
Published on: April 10, 2020
相关概念视频
Formation of Lipopolysaccharides
Gene Regulation in Microbial Communities: Quorum Sensing
Defense Against Bacterial Pathogens
Phagocytes
Phagocytes are the frontline soldiers of the immune system. They include neutrophils and macrophages. Neutrophils are the most abundant type of white blood cell and are quickly mobilized to the site of infection. Macrophages are larger cells that patrol...
Stringent Response in E. coli
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
Biosynthesis of Lipids
