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多聚磷酸激酶1与铜绿假单胞菌的眼毒性

Polyphosphate kinase 1 and the ocular virulence of Pseudomonas aeruginosa.

作者信息

Parks Quinn M, Hobden Jeffery A

机构信息

Department of Microbiology, Immunology, and Parasitology, LSU Health Sciences Center, New Orleans, Louisiana 70112, USA.

出版信息

Invest Ophthalmol Vis Sci. 2005 Jan;46(1):248-51. doi: 10.1167/iovs.04-0340.

Abstract

PURPOSE

To determine the role of polyphosphate kinase 1 (PPK1) in the ocular virulence of Pseudomonas aeruginosa.

METHODS

Using a mouse model of infection, P. aeruginosa strains PAO1, PAOM5 (an isogenic mutant of PAO1 deficient in PPK1), and PAOM5+PPK1 (the mutant complemented with PPK1 on plasmid pHEPAK11) were compared for ocular virulence. These strains were also characterized with respect to traits associated with survival and pathogenicity in an ocular environment.

RESULTS

The PPK1-deficient strain PAOM5 was significantly less virulent than either wild-type PAO1 or the complemented mutant (P <0.016). Loss of virulence was not associated with serum sensitivity or diminished adherence to the cornea. However, PAOM5 has an increased susceptibility to oxidative stress and was cleared from corneal tissue significantly better (P <0.006) than either the wild-type or restored strain. Furthermore, the PPK1-deficient mutant produced significantly less (P <0.022) pyocyanin.

CONCLUSIONS

PPK1 is essential for a successful ocular infection by P. aeruginosa. The loss of ocular virulence is probably due to the dysregulation of multiple genes, including those responsible for stress response.

摘要

目的

确定多聚磷酸激酶1(PPK1)在铜绿假单胞菌眼部毒力中的作用。

方法

使用感染小鼠模型,比较铜绿假单胞菌菌株PAO1、PAOM5(PAO1的PPK1基因缺失的同基因突变体)和PAOM5+PPK1(在质粒pHEPAK11上用PPK1互补的突变体)的眼部毒力。还对这些菌株在眼部环境中与生存和致病性相关的特征进行了表征。

结果

PPK1缺陷菌株PAOM5的毒力明显低于野生型PAO1或互补突变体(P<0.016)。毒力丧失与血清敏感性或角膜黏附力降低无关。然而,PAOM5对氧化应激的敏感性增加,并且从角膜组织中清除的速度明显快于野生型或回复菌株(P<0.006)。此外,PPK1缺陷突变体产生的绿脓菌素明显较少(P<0.022)。

结论

PPK1对铜绿假单胞菌成功的眼部感染至关重要。眼部毒力的丧失可能是由于多个基因的失调,包括那些负责应激反应的基因。

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