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Pathogens
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Signaling Systems in Pseudomonas aeruginosa Biofilm
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Signaling Systems in Pseudomonas aeruginosa Biofilm

A special issue of Pathogens (ISSN 2076-0817).

Deadline for manuscript submissions: closed (30 October 2017) | Viewed by 39761

Special Issue Editors

Prof. Dr. Tim Holm Jakobsen

E-Mail Website
Guest Editor
Costerton Biofilm Center, Faculty of Health Sciences, Department of Immunology and Microbiology, Blegdamsvej 3B, 2200 Copenhagen, Denmark
Interests: signaling systems; quorum sensing; biofilm; Pseudomonas aeruginosa; antimicrobial research; anti-virulence; quorum sensing inhibition
Prof. Jens Bo Andersen

E-Mail Website
Guest Editor
Costerton Biofilm Center, Faculty of Health Sciences, Department of Immunology and Microbiology, Blegdamsvej 3B, 2200 Copenhagen, Denmark
Interests: biofilm regulation; biofilm genetics; cell signaling reporter systems

Special Issue Information

Dear Colleagues,

Up until the 1970s, bacteria were understood to live as single organisms (planktonic mode of life), floating or actively swimming in their respective environments. This perception was challenged by the discovery that bacteria can live as organized aggregated communities, termed biofilms, and today the biofilm mode of growth is considered the favored life form of bacteria. Biofilm formation in the environment is believed to be an ancient strategy by which bacteria increase their survival potential in hostile environments. Extensive investigations support this to also be valid for biofilm related infections where the bacteria show highly elevated tolerance towards antibiotics and the immune system, compared with planktonic cells. Several signaling systems have been shown to be involved in different aspects of biofilm formation and maintenance, not least Quorum Sensing (QS) and cyclic-di-GMP. The importance of such signaling systems is supported by the growing identification of how factors regulated by these systems favor survival potentials of pathogens like Pseudomonas aeruginosa. Our knowledge of signaling systems is constantly evolving and new components taking part in the regulation are discovered.

Treatment of biofilm infections is significantly more difficult and complex compared to the relatively simple task of treating acute infections. Inhibition of signaling systems like QS and cyclic-di-GMP has gained considerable attention as potential approaches in the attempt to develop new strategies against biofilms. This Special Issue in Pathogens on “Signaling Systems in Pseudomonas aeruginosa Biofilm” centers on the newest studies and current knowledge about the influence of signaling systems on P. aeruginosa biofilm, both in vitro and in vivo, as well as on the potential of modulating these regulatory systems to lower biofilm survival. We invite you to submit a research or review manuscripts covering these important molecular aspects of P. aeruginosa biofilm and look forward to contributions that can increase our understanding and knowledge of this important scientific field.

Prof. Dr. Tim Holm Jakobsen
Prof. Jens Bo Andersen
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pathogens is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • signaling systems
  • quorum sensing
  • cyclic-di-GMP
  • Gac/rsm cascade
  • sRNAs
  • biofilm
  • virulence
  • Pseudomonas aeruginosa
  • quorum sensing inhibitors
  • cyclic-di-GMP inhibitors

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Published Papers (5 papers)

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Research

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13 pages, 4201 KiB  
Article
Inhibition of Pseudomonas aeruginosa Biofilm Formation with Surface Modified Polymeric Nanoparticles
by Tyler R. Flockton, Logan Schnorbus, Agustin Araujo, Jill Adams, Maryjane Hammel and Lark J. Perez
Pathogens 2019, 8(2), 55; https://doi.org/10.3390/pathogens8020055 - 24 Apr 2019
Cited by 31 | Viewed by 5779
Abstract
The gram-negative bacterial pathogen Pseudomonas aeruginosa represents a prominent clinical concern. Due to the observed high levels of antibiotic resistance, copious biofilm formation, and wide array of virulence factors produced by these bacteria, new treatment technologies are required. Here, we present the development [...] Read more.
The gram-negative bacterial pathogen Pseudomonas aeruginosa represents a prominent clinical concern. Due to the observed high levels of antibiotic resistance, copious biofilm formation, and wide array of virulence factors produced by these bacteria, new treatment technologies are required. Here, we present the development of a series of P. aeruginosa LecA-targeted polymeric nanoparticles and demonstrate the anti-adhesion and biofilm inhibitory properties of these constructs. Full article
(This article belongs to the Special Issue Signaling Systems in Pseudomonas aeruginosa Biofilm)
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16 pages, 9501 KiB  
Article
Different Dose-Dependent Modes of Action of C-Type Natriuretic Peptide on Pseudomonas aeruginosa Biofilm Formation
by Florie Desriac, Thomas Clamens, Thibaut Rosay, Sophie Rodrigues, Ali Tahrioui, Jérémy Enault, Lucille Roquigny, Pierre-Jean Racine, Laure Taupin, Alexis Bazire, Alain Dufour, Jérôme Leprince, Emeline Bouffartigues, Sylvie Chevalier, Marc G. J. Feuilloley and Olivier Lesouhaitier
Pathogens 2018, 7(2), 47; https://doi.org/10.3390/pathogens7020047 - 24 Apr 2018
Cited by 12 | Viewed by 4822
Abstract
We have previously shown that the C-type Natriuretic Peptide (CNP), a peptide produced by lungs, is able to impact Pseudomonas aeruginosa physiology. In the present work, the effect of CNP at different concentrations on P. aeruginosa biofilm formation was studied and the mechanisms [...] Read more.
We have previously shown that the C-type Natriuretic Peptide (CNP), a peptide produced by lungs, is able to impact Pseudomonas aeruginosa physiology. In the present work, the effect of CNP at different concentrations on P. aeruginosa biofilm formation was studied and the mechanisms of action of this human hormone on P. aeruginosa were deciphered. CNP was shown to inhibit dynamic biofilm formation in a dose-dependent manner without affecting the bacterial growth at any tested concentrations. The most effective concentrations were 1 and 0.1 µM. At 0.1 µM, the biofilm formation inhibition was fully dependent on the CNP sensor protein AmiC, whereas it was only partially AmiC-dependent at 1 µM, revealing the existence of a second AmiC-independent mode of action of CNP on P. aeruginosa. At 1 µM, CNP reduced both P. aeruginosa adhesion on glass and di-rhamnolipid production and also increased the bacterial membrane fluidity. The various effects of CNP at 1 µM and 0.1 µM on P. aeruginosa shown here should have major consequences to design drugs for biofilm treatment or prevention. Full article
(This article belongs to the Special Issue Signaling Systems in Pseudomonas aeruginosa Biofilm)
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3039 KiB  
Article
PqsA Promotes Pyoverdine Production via Biofilm Formation
by Donghoon Kang, Kelly E. Turner and Natalia V. Kirienko
Pathogens 2018, 7(1), 3; https://doi.org/10.3390/pathogens7010003 - 25 Dec 2017
Cited by 39 | Viewed by 7347
Abstract
Biofilms create an impermeable barrier against antimicrobial treatment and immune cell access, severely complicating treatment and clearance of nosocomial Pseudomonas aeruginosa infections. We recently reported that biofilm also contributes to pathogen virulence by regulating the production of the siderophore pyoverdine. In this study, [...] Read more.
Biofilms create an impermeable barrier against antimicrobial treatment and immune cell access, severely complicating treatment and clearance of nosocomial Pseudomonas aeruginosa infections. We recently reported that biofilm also contributes to pathogen virulence by regulating the production of the siderophore pyoverdine. In this study, we investigated the role of PqsA, a key cell-signaling protein, in this regulatory pathway. We demonstrate that PqsA promotes pyoverdine production in a biofilm-dependent manner. Under nutritionally deficient conditions, where biofilm and pyoverdine are decoupled, PqsA is dispensable for pyoverdine production. Interestingly, although PqsA-dependent pyoverdine production does not rely upon Pseudomonas quinolone signal (PQS) biosynthesis, exogenous PQS can also trigger biofilm-independent production of pyoverdine. Adding PQS rapidly induced planktonic cell aggregation. Moreover, these clumps of cells exhibit strong expression of pyoverdine biosynthetic genes and show substantial production of this siderophore. Finally, we surveyed the relationship between biofilm formation and pyoverdine production in various clinical and environmental isolates of P. aeruginosa to evaluate the clinical significance of targeting biofilm during infections. Our findings implicate PqsA in P. aeruginosa virulence by regulating biofilm formation and pyoverdine production. Full article
(This article belongs to the Special Issue Signaling Systems in Pseudomonas aeruginosa Biofilm)
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3860 KiB  
Article
Characterization of Three Ocular Clinical Isolates of P. aeruginosa: Viability, Biofilm Formation, Adherence, Infectivity, and Effects of Glycyrrhizin
by Xudong Peng, Sandamali A. Ekanayaka, Sharon A. McClellan, Ronald P. Barrett, Kerry Vistisen and Linda D. Hazlett
Pathogens 2017, 6(4), 52; https://doi.org/10.3390/pathogens6040052 - 24 Oct 2017
Cited by 17 | Viewed by 4746
Abstract
We selectively characterized three isolates from Pseudomonas aeruginosa keratitis patients and how glycyrrhizin (GLY) affected them. Type III toxins were determined using polymerase chain reaction (PCR). Minimum Inhibitory Concentration (MIC) of GLY and assays for its effects on: time kill, bacterial permeability, and [...] Read more.
We selectively characterized three isolates from Pseudomonas aeruginosa keratitis patients and how glycyrrhizin (GLY) affected them. Type III toxins were determined using polymerase chain reaction (PCR). Minimum Inhibitory Concentration (MIC) of GLY and assays for its effects on: time kill, bacterial permeability, and biofilm/adhesion were done. In vivo, C57BL/6 (B6) mice were treated topically with GLY after G81007 infection. Clinical score, photography with a slit lamp and RT-PCR were used to assess treatment effects. Isolates expressed exoS and exoT, but not exoU. MIC for all isolates was 40 mg/mL GLY and bacteriostatic effects were seen for G81007 after treatment using time kill assays. From viability testing, GLY treatment significantly increased the number of permeabilized bacteria (live/dead assay). Isolates 070490 and G81007 formed more biofilms compared with R59733 and PAO1 (control). GLY-treated bacteria had diminished biofilm compared with controls for all isolates. GLY reduced adherence of the G81007 isolate to cultured cells and affected specific biofilm associated systems tested by reverse transcription PCR (RT-PCR). In vivo, after G81007 infection, GLY treatment reduced clinical score and messenger RNA (mRNA) expression of IL-1β, TNF-α, CXCL2 and HMGB1. This study provides evidence that GLY is bacteriostatic for G81007. It also affects biofilm production, adherence to cultured cells, and an improved keratitis outcome. Full article
(This article belongs to the Special Issue Signaling Systems in Pseudomonas aeruginosa Biofilm)
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Review

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603 KiB  
Review
An Update on the Sociomicrobiology of Quorum Sensing in Gram-Negative Biofilm Development
by Daniel Passos da Silva, Melissa C. Schofield, Matthew R. Parsek and Boo Shan Tseng
Pathogens 2017, 6(4), 51; https://doi.org/10.3390/pathogens6040051 - 21 Oct 2017
Cited by 98 | Viewed by 16180
Abstract
Bacteria are social creatures that are able to interact and coordinate behaviors with each other in a multitude of ways. The study of such group behaviors in microbes was coined “sociomicrobiology” in 2005. Two such group behaviors in bacteria are quorum sensing (QS) [...] Read more.
Bacteria are social creatures that are able to interact and coordinate behaviors with each other in a multitude of ways. The study of such group behaviors in microbes was coined “sociomicrobiology” in 2005. Two such group behaviors in bacteria are quorum sensing (QS) and biofilm formation. At a very basic level, QS is the ability to sense bacterial density via cell-to-cell signaling using self-produced signals called autoinducers, and biofilms are aggregates of cells that are attached to one another via a self-produced, extracellular matrix. Since cells in biofilm aggregates are in close proximity, biofilms represent an ecologically relevant environment for QS. While QS is known to affect biofilm formation in both Gram-negative and Gram-positive species, in this review, we will focus exclusively on Gram-negative bacteria, with an emphasis on Pseudomonas aeruginosa. We will begin by describing QS systems in P. aeruginosa and how they affect P. aeruginosa biofilm formation. We then expand our review to other Gram-negative bacteria and conclude with interesting questions with regard to the effect of biofilms on QS. Full article
(This article belongs to the Special Issue Signaling Systems in Pseudomonas aeruginosa Biofilm)
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