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swarm 运动对铜绿假单胞菌小鼠皮肤脓肿感染模型传播的贡献。

Contribution of Swarming Motility to Dissemination in a Pseudomonas aeruginosa Murine Skin Abscess Infection Model.

机构信息

Centre for Microbial Diseases and Immunity Research, Department of Microbiology and Immunology, University of British Columbia, Vancouver, Canada.

Department of Microbiology and Immunology, University of Otago, Dunedin, New Zealand.

出版信息

J Infect Dis. 2021 Aug 16;224(4):726-733. doi: 10.1093/infdis/jiaa778.

Abstract

Swarming motility in Pseudomonas aeruginosa is a multicellular adaptation induced by semisolid medium with amino acids as a nitrogen source. By phenotypic screening, we differentiated swarming from other complex adaptive phenotypes, such as biofilm formation, swimming and twitching, by identifying a swarming-specific mutant in ptsP, a metabolic regulator. This swarming-deficient mutant was tested in an acute murine skin abscess infection model. Bacteria were recovered at significantly lower numbers from organs of mice infected with the ∆ptsP mutant. We also tested the synthetic peptide 1018 for activity against different motilities and efficacy in vivo. Treatment with peptide 1018 mimicked the phenotype of the ∆ptsP mutant in vitro, as swarming was inhibited at low concentrations (<2 μg/mL) but not swimming or twitching, and in vivo, as mice had a reduced bacterial load recovered from organs. Therefore, PtsP functions as a regulator of swarming, which in turn contributes to dissemination and colonization in vivo.

摘要

铜绿假单胞菌的群集运动是一种由含有氨基酸作为氮源的半固体培养基诱导的多细胞适应现象。通过表型筛选,我们从其他复杂的适应表型(如生物膜形成、游泳和抽搐)中区分出群集运动,方法是在代谢调节剂 ptsP 中鉴定出一个群集运动特异性突变体。在急性鼠皮肤脓肿感染模型中测试了这个缺乏群集运动的突变体。与感染 ∆ptsP 突变体的小鼠相比,从感染器官中回收的细菌数量明显减少。我们还测试了合成肽 1018 对不同运动性的活性和体内功效。用肽 1018 处理在体外模拟了 ∆ptsP 突变体的表型,因为在低浓度(<2 μg/mL)下抑制了群集运动,但不抑制游泳或抽搐运动,在体内,从器官中回收的细菌负荷减少。因此,PtsP 作为群集运动的调节剂发挥作用,这反过来又有助于在体内的传播和定植。

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