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伪白 aeruginosa 中的 ExoS 效应器过活 III 型分泌系统突变促进中性粒细胞中增强的血膜破裂

Arianna D Reuven¹, Bethany W Mwaura¹, James B Bliska¹

¹Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth College, Hanover, NH, USA.

bioRxiv : the preprint server for biology

|February 8, 2024

概括

伪omonas空气菌伪omonas空气菌

科学领域:

微生物学微生物学
免疫学免疫学免疫学
病原发生和发病的过程.

背景情况:

Pseudomonas aeruginosa 是机会性感染的主要原因,特别是在囊性纤维化患者中.
第三类分泌系统 (T3SS) 和其效应器ExoS是关键的毒性因素.
ExoS 抑制了宿主免疫反应,如细胞分裂和氧化突发.

研究的目的:

为了研究ExoS ADP 核糖转移酶 (ADPRT) 活性在高病毒性P. aeruginosa分离物中的作用.
确定EXOS对NLRC4炎症酶激活和中性粒细胞反应的影响.
探索由高病毒性P. aeruginosa引起的中性粒细胞损伤的机制.

主要方法:

中性粒细胞感染P. aeruginosa菌株 (PAO1和高病毒性CF分离物).
使用了野生型和转基因小鼠 (CF基因型,炎症酶缺乏).
测试了NLRC4炎症酶激活,基因素素化 (CitH3),核DNA脱凝和血膜破裂 (PMR).

主要成果:

一种具有过度活性T3SS的高毒性P. aeruginosa分离物表现出对杀死中性粒细胞的增强抵抗力.
在这种分离物中,exoS ADPRT活性促进了组素H3的素化和血膜破裂 (PMR).
补充甘氨酸抑制了PMR,这表明ninjurin-1参与其中.

结论:

增强的中性粒细胞PMR是一种新型的病原性机制,在高病毒性P. aeruginosa中,ExoS ADPRT是一种新型的病原性机制.
ExoS有助于免疫逃避和宿主细胞损伤.
宁林-1可能是针对P. aeruginosa感染的治疗干预的目标.

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