Universal soldier: Pseudomonas aeruginosa — an opportunistic generalist

Gross, Jeremy; Passmore, Ian J.; Chung, Jade C. S.; Rzhepishevska, Olena; Ramstedt, Madeleine; Welch, Martin

doi:10.1007/s11515-013-1267-x

Cited by 3 publications

(5 citation statements)

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“…Perhaps the best characterised infection scenario is in people with the inherited genetic disorder, cystic fibrosis (CF). For reasons that are still not entirely clear, people with CF appear to be exquisitely predisposed to PA infection [28,29]. These CF-associated infections are treated with aggressive antibiotic interventions, yet resistance to these agents eventually becomes all but inevitable [30].…”

Section: Pseudomonas Aeruginosa Does Things Differentlymentioning

confidence: 99%

The methylation-independent mismatch repair machinery in Pseudomonas aeruginosa

Welch

2021

Microbiology

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Over the last 70 years, we’ve all gotten used to an Escherichia coli -centric view of the microbial world. However, genomics, as well as the development of improved tools for genetic manipulation in other species, is showing us that other bugs do things differently, and that we cannot simply extrapolate from E. coli to everything else. A particularly good example of this is encountered when considering the mechanism(s) involved in DNA mismatch repair by the opportunistic human pathogen, Pseudomonas aeruginosa (PA). This is a particularly relevant phenotype to examine in PA, since defects in the mismatch repair (MMR) machinery often give rise to the property of hypermutability. This, in turn, is linked with the vertical acquisition of important pathoadaptive traits in the organism, such as antimicrobial resistance. But it turns out that PA lacks some key genes associated with MMR in E. coli , and a closer inspection of what is known (or can be inferred) about the MMR enzymology reveals profound differences compared with other, well-characterized organisms. Here, we review these differences and comment on their biological implications.

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Section: Pseudomonas Aeruginosa Does Things Differentlymentioning

confidence: 99%

The methylation-independent mismatch repair machinery in Pseudomonas aeruginosa

Welch

2021

Microbiology

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“…The γ-proteobacterium Pseudomonas aeruginosa thrives in various aquatic and terrestrial habitats [1], as well as in multiple niches in the human host such as the lungs, eyes and ears [2][3][4].…”

Section: Introductionmentioning

confidence: 99%

“…In particular, P. aeruginosa is a major threat to artificially ventilated patients [8] and those with cystic fibrosis (CF), of which roughly 60% are chronically infected by P. aeruginosa [9]. P. aeruginosa displays high metabolic versatility, enabling it to infect and persist in different human tissues and organs [2]. As an example, it has been found that P. aeruginosa adapts its iron uptake strategies depending on the type of infection [10].…”

Section: Introductionmentioning

confidence: 99%

“…The

-proteobacterium Pseudomonas aeruginosa thrives in various aquatic and terrestrial habitats [ 1 ], as well as in multiple niches in the human host such as the lungs, eyes and ears [ 2 , 3 , 4 ]. Its affinity and ability to form biofilms on surfaces enables this bacterium to colonize burn wounds and the surfaces of invasive medical devices such as catheters and implants [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

“…P. aeruginosa displays high metabolic versatility, enabling it to infect and persist in different human tissues and organs [ 2 ]. As an example, it has been found that P. aeruginosa adapts its iron uptake strategies depending on the type of infection [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

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Untargeted LC-MS Metabolomics Differentiates Between Virulent and Avirulent Clinical Strains of Pseudomonas aeruginosa

et al. 2020

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Pseudomonas aeruginosa is a facultative pathogen that can cause, inter alia, acute or chronic pneumonia in predisposed individuals. The gram-negative bacterium displays considerable genomic and phenotypic diversity that is also shaped by small molecule secondary metabolites. The discrimination of virulence phenotypes is highly relevant to the diagnosis and prognosis of P. aeruginosa infections. In order to discover small molecule metabolites that distinguish different virulence phenotypes of P. aeruginosa, 35 clinical strains were cultivated under standard conditions, characterized in terms of virulence and biofilm phenotype, and their metabolomes were investigated by untargeted liquid chromatography—mass spectrometry. The data was both mined for individual candidate markers as well as used to construct statistical models to infer the virulence phenotype from metabolomics data. We found that clinical strains that differed in their virulence and biofilm phenotype also had pronounced divergence in their metabolomes, as underlined by 332 features that were significantly differentially abundant with fold changes greater than 1.5 in both directions. Important virulence-associated secondary metabolites like rhamnolipids, alkyl quinolones or phenazines were found to be strongly upregulated in virulent strains. In contrast, we observed little change in primary metabolism. A hitherto novel cationic metabolite with a sum formula of C12H15N2 could be identified as a candidate biomarker. A random forest model was able to classify strains according to their virulence and biofilm phenotype with an area under the Receiver Operation Characteristics curve of 0.84. These findings demonstrate that untargeted metabolomics is a valuable tool to characterize P. aeruginosa virulence, and to explore interrelations between clinically important phenotypic traits and the bacterial metabolome.

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