The role of pyocyanin in Pseudomonas aeruginosa infection

Lau, Gee W.; Hassett, Daniel J.; Ran, Huimin; Kong, Fanrong

doi:10.1016/j.molmed.2004.10.002

Cited by 625 publications

(606 citation statements)

References 56 publications

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“…These compounds are known for their toxicity in other bacteria (Baron and Rowe, 1981) and in eukaryotes ranging from nematodes to humans (Ran et al, 2003;Lau et al, 2004;Mavrodi et al, 2006;Morales et al, 2010;Morales et al, 2013).…”

Section: Interspecies Competition Triggers Virulencementioning

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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Section: Interspecies Competition Triggers Virulencementioning

confidence: 99%

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

et al. 2014

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“…P. aeruginosa has developed highly sophisticated virulence mechanisms and secretes a wide range of extracellular virulence factors, such as proteases (50), exotoxin A (53), rhamnolipids (23), pyocyanin (24), and siderophores (11). Production of these virulence factors is regulated to a large extent by a cell density-dependent gene regulatory mechanism termed quorum sensing (QS) (35).…”

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confidence: 99%

Anaerobiosis-Induced Loss of Cytotoxicity Is Due to Inactivation of Quorum Sensing in Pseudomonas aeruginosa

et al. 2011

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Pseudomonas aeruginosa, an opportunistic pathogen of clinical importance, causes chronic airway infections in patients with cystic fibrosis (CF). Current literature suggests that pockets with reduced oxygen tension exist in the CF airway mucus. However, virulence features of this opportunistic pathogen under such conditions are largely unknown. Cell-free supernatant of the standard laboratory P. aeruginosa strain PAO1 obtained from anaerobic culture, but not aerobic culture, failed to kill A549 human airway epithelial cells. Further investigation revealed that this reduced cytotoxicity upon anaerobiosis was due to the suppressed secretion of elastase, a virulence factor controlled by P. aeruginosa quorum sensing (QS). Both a lacZ-reporter fusion assay and quantitative real-time PCR (RT-PCR) analysis demonstrated that transcription of the elastase-encoding lasB gene was substantially decreased during anaerobic growth compared with aerobic growth. Moreover, transcription of other genes controlled by the LasI/R QS system, such as rhlR, vqsR, mvfR, and rsaL, was also repressed under the same anaerobic growth conditions. Importantly, synthesis of 3-oxo-C 12 -HSL (PAI-1), an autoinducer molecule that mediates induction of the LasI/R QS system, was >22-fold decreased during anaerobic growth while C 4 -HSL (PAI-2), which mediates RhlI/R QS, was nondetectable under the same growth conditions. Transcription of the lasB gene was restored by exogenous supplementation with autoinducers, with PAI-2 more effective than PAI-1 or Pseudomonas quinolone signal (PQS) at restoring transcription of the lasB gene. Together, these results suggest that anaerobiosis deprives P. aeruginosa of the ability to regulate its virulence via QS and this misregulation attenuates the pathogenic potential of this important pathogen.

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“…The pigmentation of P. aeruginosa is the result of the production of different pigments such as pyocyanin and other phenazines, as well as pyoverdine, pyomelanin and pyorubin (Lau et al, 2004;Visca et al, 2007;Rodríguez-Rojas et al, 2009;Jayaseelan et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

“…P. aeruginosa is also a well-known opportunistic pathogen that may negatively affect infected patients due to its ability to produce many virulence factors. Among the P. aeruginosa virulence factors, pigments such as pyocyanin, a water-soluble blue and non-fluorescent phenazine (Lau et al, 2004;Jayaseelan et al, 2014), pyoverdine, a fluorescent siderophore playing an important role in iron uptake (Visca et al, 2007), pyorubin and pyomelanin, non-fluorescent red and brown pigments (Rodríguez-Rojas et al, 2009), play an important role. Concern regarding P. aeruginosa is mainly due to its resistance to many antibiotics and its tolerance to disinfectants and antimicrobial treatments (Jimenez et al, 2012;Morita et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Pigments influence the tolerance of Pseudomonas aeruginosa PAO1 to photodynamically induced oxidative stress

et al. 2015

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Pseudomonas aeruginosa is an opportunistic pathogen known to be resistant to different classes of antibiotics and disinfectants. P. aeruginosa also displays a certain degree of tolerance to photodynamic therapy (PDT), an alternative antimicrobial approach exploiting a photo-oxidative stress induced by exogenous photosensitizers and visible light. To evaluate whether P. aeruginosa pigments can contribute to its relative tolerance to PDT, we analysed the response to this treatment of isogenic transposon mutants of P. aeruginosa PAO1 with altered pigmentation. In general, in the presence of pigments a higher tolerance to PDT-induced photooxidative stress was observed. Hyperproduction of pyomelanin makes the cells much more tolerant to stress caused by either radicals or singlet oxygen generated by different photosensitizers upon photoactivation. Phenazines, pyocyanin and phenazine-1-carboxylic acid, produced in different amounts depending on the cultural conditions, are able to counteract both types of PDT-elicited reactive oxygen species. Hyperproduction of pyoverdine, caused by a mutation in a quorum-sensing gene, rendered P. aeruginosa more tolerant to a photosensitizer that generates mainly singlet oxygen, although in this case the observed tolerance to photooxidative stress cannot be exclusively attributed to the presence of the pigment.

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The role of pyocyanin in Pseudomonas aeruginosa infection

Cited by 625 publications

References 56 publications

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

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

Anaerobiosis-Induced Loss of Cytotoxicity Is Due to Inactivation of Quorum Sensing in Pseudomonas aeruginosa

Pigments influence the tolerance of Pseudomonas aeruginosa PAO1 to photodynamically induced oxidative stress

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