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转录基因分析揭示了RetS介导的VI型分泌系统和宿主细胞响应在Pseudomonas aeruginosa感染中的调节

Yinglin Wu^1,2,3, Shan Huang^1,2,3, Kai Zhang⁴

¹The Second Clinical Medical College, Guangzhou University of Chinese Medicine, State Key Laboratory of Traditional Chinese Medicine Syndrome, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, China.

Frontiers in cellular and infection microbiology

|June 25, 2025

概括

Pseudomonas aeruginosa 的第六类分泌系统 (T6SS) 通过激活宿主 PDE4C 途径来驱动慢性感染. 抑制PDE4C可减少T6SS诱导的炎症和细胞损伤,提供治疗潜力.

科学领域:

微生物学和免疫学
分子生物学分子生物学
病原体与宿主之间的相互作用

背景情况:

Pseudomonas aeruginosa 是一种机会性病原体,导致慢性感染,特别是在囊性纤维化和 COPD 患者中.
第六类分泌系统 (T6SS) 是P. aeruginosa慢性感染的关键毒性因素.

研究的目的:

为了阐明P. aeruginosa感染中T6SS的调节机制.
研究T6SS对宿主细胞的致病作用.
为了确定T6SS介导炎症的潜在治疗点.

主要方法:

转录组测序 (RNA-Seq) 的P. aeruginosa和宿主上皮细胞.
构建和分析P. aeruginosa的删除突变体 (ΔretS, ΔcupC, ΔhptC-PA0034, ΔclpV1ΔclpV2).这些突变体的结构和分析.
功能性检测包括细胞毒性,粘附性和炎症标记物量化 (IL-1β,IL-6,TNF-α).

主要成果:

在P. aeruginosa中,T6SS表达因慢性感染而升高,并通过retS删除激活.
CupC 膜增强 T6SS 接触杀伤; hptC-PA0034 调节 cupC 的表达.
在上皮细胞中PDE4C通路的T6SS激活增加了细胞死亡和炎症; PDE抑制剂减轻了这些影响.

结论:

通过调节宿主细胞信号传递,特别是PDE4C通路,T6SS在P. aeruginosa毒性中发挥着关键作用.
针对T6SS及其下游效应,如PDE4C激活,为P. aeruginosa感染提供了一个有希望的治疗策略.
了解T6SS调节和宿主相互作用对于开发有效治疗慢性P. aeruginosa感染至关重要.

关键词:

A549上皮细胞上皮细胞在CUPC FIMBRIE中使用.这是一个PDE4C.伪omonas空气菌伪omonas空气菌陪伴者-使用者路径.第六类分泌系统.毒性毒性是一种毒性.

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