Anticandidal activity of <i>Pseudomonas aeruginosa</i> strains isolated from clinical specimens

Kaleli, İlknur; Cevahir, Nural; Demir, Melek; Yildirim, Umut; Sahin, Rasim

doi:10.1111/j.1439-0507.2006.01322.x

Cited by 38 publications

(29 citation statements)

References 16 publications

(59 reference statements)

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“…The first is based on the observation that virulent P. aeruginosa strains; including PA14 kill yeast [54],[55],[56]; and the second is based on that P. aeruginosa can infect and kill Drosophila melanogaster [57],[58],[59], and that mvfR mutant cells exhibit attenuated virulence in flies [57]. As illustrated in Figure 1C–D, a zone of yeast growth inhibition was observed around PA14, but not around the mvfR − , or pqsE − mutants following plating of C. neoformans KN99α 5 mm from the bacterial colony on a YPD plate (Figure 1D).…”

Section: Resultsmentioning

confidence: 99%

Homeostatic Interplay between Bacterial Cell-Cell Signaling and Iron in Virulence

et al. 2010

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Pathogenic bacteria use interconnected multi-layered regulatory networks, such as quorum sensing (QS) networks to sense and respond to environmental cues and external and internal bacterial cell signals, and thereby adapt to and exploit target hosts. Despite the many advances that have been made in understanding QS regulation, little is known regarding how these inputs are integrated and processed in the context of multi-layered QS regulatory networks. Here we report the examination of the Pseudomonas aeruginosa QS 4-hydroxy-2-alkylquinolines (HAQs) MvfR regulatory network and determination of its interaction with the QS acyl-homoserine-lactone (AHL) RhlR network. The aim of this work was to elucidate paradigmatically the complex relationships between multi-layered regulatory QS circuitries, their signaling molecules, and the environmental cues to which they respond. Our findings revealed positive and negative homeostatic regulatory loops that fine-tune the MvfR regulon via a multi-layered dependent homeostatic regulation of the cell-cell signaling molecules PQS and HHQ, and interplay between these molecules and iron. We discovered that the MvfR regulon component PqsE is a key mediator in orchestrating this homeostatic regulation, and in establishing a connection to the QS rhlR system in cooperation with RhlR. Our results show that P. aeruginosa modulates the intensity of its virulence response, at least in part, through this multi-layered interplay. Our findings underscore the importance of the homeostatic interplay that balances competition within and between QS systems via cell-cell signaling molecules and environmental cues in the control of virulence gene expression. Elucidation of the fine-tuning of this complex relationship offers novel insights into the regulation of these systems and may inform strategies designed to limit infections caused by P. aeruginosa and related human pathogens.

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Section: Resultsmentioning

confidence: 99%

Homeostatic Interplay between Bacterial Cell-Cell Signaling and Iron in Virulence

et al. 2010

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“…In this study, we used the term ‘mixed Candida /bacterial BSI’ to describe the isolation of bacterial species within 48 h of the time of candidaemia to avoid confusion with previous studies. We chose this definition because concomitant bacteraemia may obscure the detection of fungaemia using standard blood culture techniques by suppression of fungal growth [9,10,26]. The inclusion of only synchronous candidaemia and bacteraemia could cause the underestimation of the incidence of mixed Candida /bacterial BSIs.…”

Section: Discussionmentioning

confidence: 99%

Risk factors for and clinical implications of mixed Candida/bacterial bloodstream infections

Kim¹,

Yoon²,

Kim³

et al. 2013

Clinical Microbiology and Infection

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Mixed Candida/bacterial bloodstream infections (BSIs) have been reported to occur in more than 23% of all episodes of candidaemia. However, the clinical implications of mixed Candida/bacterial BSIs are not well known. We performed a retrospective case-control study of all consecutive patients with candidaemia over a 5-year period to determine the risk factors for and clinical outcomes of mixed Candida/bacterial BSIs (cases) compared with monomicrobial candidaemia (controls). Thirty-seven (29%) out of 126 patients with candidaemia met the criteria for cases. Coagulase-negative staphylococci were the predominant bacteria (23%) in cases. In multivariate analysis, duration of previous hospital stay ≥7 weeks (odds ratio (OR), 2.86; 95% confidence interval (CI), 1.09–7.53), prior antibiotic therapy ≥7 days (OR, 0.33; 95% CI, 0.14–0.82) and septic shock at the time of candidaemia (OR, 2.60; 95% CI, 1.14–5.93) were significantly associated with cases. Documented clearance of candidaemia within 3 days after initiation of antifungal therapy was less frequent in cases (63% vs. 84%; p = 0.035). The difference in the rate of treatment failure at 2 weeks was not significant between cases (68%) and controls (62%; p = 0.55). The crude mortality at 6 weeks and survival through 100 days did not differ between the two patient groups (p = 0.56 and p = 0.80, respectively). Mixed Candida/bacterial BSIs showed a lower clearance rate of candidaemia during the early period of antifungal therapy, although the treatment response and survival rate were similar regardless of concurrent bacteraemia. Further studies on the clinical relevance of species-specific Candida-bacterial interactions are needed.

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“…Both morphological forms are important for virulence, and the ability to undergo morphological transformation is therefore an important virulence trait (Gow, 1997;Calderone and Fonzi, 2001;Gow et al, 2002;Liu, 2002;Whiteway and Oberholzer, 2004). Several studies have suggested that P. aeruginosa may inhibit C. albicans growth within the host (Bauernfeind et al, 1987;Kerr, 1994;Burns et al, 1999;Gupta et al, 2005;Kaleli et al, 2007). Hogan and Kolter (2002) demonstrated that P. aeruginosa is cytotoxic to the filamentous form of C. albicans but is unable to attach to or kill C. albicans yeast cells.…”

Section: Introductionmentioning

confidence: 99%

Interspecies competition triggers virulence and mutability in Candida albicans–Pseudomonas aeruginosa mixed biofilms

et al. 2014

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Inter-kingdom and interspecies interactions are ubiquitous in nature and are important for the survival of species and ecological balance. The investigation of microbe-microbe interactions is essential for understanding the in vivo activities of commensal and pathogenic microorganisms. Candida albicans, a polymorphic fungus, and Pseudomonas aeruginosa, a Gram-negative bacterium, are two opportunistic pathogens that interact in various polymicrobial infections in humans. To determine how P. aeruginosa affects the physiology of C. albicans and vice versa, we compared the proteomes of each species in mixed biofilms versus single-species biofilms. In addition, extracellular proteins were analyzed. We observed that, in mixed biofilms, both species showed differential expression of virulence proteins, multidrug resistance-associated proteins, proteases and cell defense, stress and iron-regulated proteins. Furthermore, in mixed biofilms, both species displayed an increase in mutability compared with monospecific biofilms. This characteristic was correlated with the downregulation of enzymes conferring protection against DNA oxidation. In mixed biofilms, P. aeruginosa regulates its production of various molecules involved in quorum sensing and induces the production of virulence factors (pyoverdine, rhamnolipids and pyocyanin), which are major contributors to the ability of this bacterium to cause disease. Overall, our results indicate that interspecies competition between these opportunistic pathogens enhances the production of virulence factors and increases mutability and thus can alter the course of hostpathogen interactions in polymicrobial infections.

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Anticandidal activity of Pseudomonas aeruginosa strains isolated from clinical specimens

Cited by 38 publications

References 16 publications

Homeostatic Interplay between Bacterial Cell-Cell Signaling and Iron in Virulence

Homeostatic Interplay between Bacterial Cell-Cell Signaling and Iron in Virulence

Risk factors for and clinical implications of mixed Candida/bacterial bloodstream infections

Interspecies competition triggers virulence and mutability in Candida albicans–Pseudomonas aeruginosa mixed biofilms

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