Correlation of phenotypic and genotypic virulence markers, antimicrobial susceptibility pattern, and outcome of Pseudomonas aeruginosa sepsis infection

Juliana, Alamu; Leela, K.V.; Venkatesan, Balamurali; Thulukanam, Jayaprakash

doi:10.1016/j.micpath.2022.105716

Cited by 7 publications

(4 citation statements)

References 30 publications

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“…Beyond virulence-related factors, such as QS, flagella [33] and formation of biofilm, whose matrix proteome is enriched in proteins involved in oxidation-reduction processes, proteolysis, and transmembrane transport [34], the virulence of P. aeruginosa can also be controlled by multiple biological factors. These factors include pyoverdine production (siderophore), lasR gene presence, capsule, alginate D, elastase B, exotoxin A and Transcription factors (TFs), with noticeable regulatory roles during pathogenesis [35][36][37]. For example, RsaL, QscR, RhlR, CdpR, MvfR, PchR, PhoB and LasR were functionally unveiled as master regulators of QS, ExsA was notified as the master regulator of T3SS, and GacA was described as a key regulator of T6SS [37].…”

Section: Pathogenesis Of Pseudomonas Aeruginosamentioning

confidence: 99%

Recent advances in therapeutic targets identification and development of treatment strategies towards Pseudomonas aeruginosa infections

et al. 2023

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The opportunistic human pathogen Pseudomonas aeruginosa is the causal agent of a wide variety of infections. This non-fermentative Gram-negative bacillus can colonize zones where the skin barrier is weakened, such as wounds or burns. It also causes infections of the urinary tract, respiratory system or bloodstream. P. aeruginosa infections are common in hospitalized patients for which multidrug-resistant, respectively extensively drug-resistant isolates can be a strong contributor to a high rate of in-hospital mortality. Moreover, chronic respiratory system infections of cystic fibrosis patients are especially concerning, since very tedious to treat. P. aeruginosa exploits diverse cell-associated and secreted virulence factors, which play essential roles in its pathogenesis. Those factors encompass carbohydrate-binding proteins, quorum sensing that monitor the production of extracellular products, genes conferring extensive drug resistance, and a secretion system to deliver effectors to kill competitors or subvert host essential functions. In this article, we highlight recent advances in the understanding of P. aeruginosa pathogenicity and virulence as well as efforts for the identification of new drug targets and the development of new therapeutic strategies against P. aeruginosa infections. These recent advances provide innovative and promising strategies to circumvent infection caused by this important human pathogen.

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Section: Pathogenesis Of Pseudomonas Aeruginosamentioning

confidence: 99%

Recent advances in therapeutic targets identification and development of treatment strategies towards Pseudomonas aeruginosa infections

et al. 2023

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“…The expression of these proteases is highly influenced by environmental factors such as the availability of nutrients, pH, and temperature, as well as the phase of the cell cycle or the type of growth (planktonic or biofilm). In general, its production is higher in acute infections such as bacteremia and acute pneumonia compared with chronic infections, suggesting a role in the initial colonization of tissues [ 75 , 76 ].…”

Section: Complement Evasion Strategies Of P Aeruginosamentioning

confidence: 99%

Pseudomonas aeruginosa and the Complement System: A Review of the Evasion Strategies

et al. 2023

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The increasing emergence of multidrug resistant isolates of P. aeruginosa causes major problems in hospitals worldwide. This concern is particularly significant in bloodstream infections that progress rapidly, with a high number of deaths within the first hours and without time to select the most appropriate treatment. In fact, despite improvements in antimicrobial therapy and hospital care, P. aeruginosa bacteremia remains fatal in about 30% of cases. The complement system is a main defensive mechanism in blood against this pathogen. This system can mark bacteria for phagocytosis or directly lyse it via the insertion of a membrane attack complex in the bacterial membrane. P. aeruginosa exploits different strategies to resist complement attack. In this review for the special issue on “bacterial pathogens associated with bacteriemia”, we present an overview of the interactions between P. aeruginosa and the complement components and strategies used by this pathogen to prevent recognition and killing by the complement system. A thorough understanding of these interactions will be critical in order to develop drugs to counteract bacterial evasion mechanisms.

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“…The protease elastase encoded by lasB, secreted under the control of 3-Oxo-C12-HSL, plays an important role during P. aeruginosa infection, in particular in the initial phase of colonization of tissues with its capacity to degrade and inactivate components of the complement immune system [43].…”

Section: Effect Of Sacpox On Liquid Pao1 Culture: Growth and Pathogen...mentioning

confidence: 99%

Thermostable Lactonases Inhibit Pseudomonas aeruginosa Biofilm: Effect In Vitro and in Drosophila melanogaster Model of Chronic Infection

Porzio,

Andrenacci,

Manco

2023

IJMS

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Pseudomonas aeruginosa is one of the six antimicrobial-resistant pathogens known as “ESKAPE” that represent a global threat to human health and are considered priority targets for the development of novel antimicrobials and alternative therapeutics. The virulence of P. aeruginosa is regulated by a four-chemicals communication system termed quorum sensing (QS), and one main class of QS signals is termed acylhomoserine lactones (acyl-HSLs), which includes 3-Oxo-dodecanoil homoserine lactone (3-Oxo-C12-HSL), which regulates the expression of genes implicated in virulence and biofilm formation. Lactonases, like Paraoxonase 2 (PON2) from humans and the phosphotriesterase-like lactonases (PLLs) from thermostable microorganisms, are able to hydrolyze acyl-HSLs. In this work, we explored in vitro and in an animal model the effect of some lactonases on the production of Pseudomonas virulence factors. This study presents a model of chronic infection in which bacteria were administered by feeding, and Drosophila adults were treated with enzymes and the antibiotic tobramycin, alone or in combination. In vitro, we observed significant effects of lactonases on biofilm formation as well as effects on bacterial motility and the expression of virulence factors. The treatment in vivo by feeding with the lactonase SacPox allowed us to significantly increase the biocidal effect of tobramycin in chronic infection.

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Correlation of phenotypic and genotypic virulence markers, antimicrobial susceptibility pattern, and outcome of Pseudomonas aeruginosa sepsis infection

Cited by 7 publications

References 30 publications

Recent advances in therapeutic targets identification and development of treatment strategies towards Pseudomonas aeruginosa infections

Recent advances in therapeutic targets identification and development of treatment strategies towards Pseudomonas aeruginosa infections

Pseudomonas aeruginosa and the Complement System: A Review of the Evasion Strategies

Thermostable Lactonases Inhibit Pseudomonas aeruginosa Biofilm: Effect In Vitro and in Drosophila melanogaster Model of Chronic Infection

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