Journal articles: 'Pseudomonas aeruginosa PA14'

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Choi, Ji Young, Costi D. Sifri, Boyan C. Goumnerov, Laurence G. Rahme, Frederick M. Ausubel, and Stephen B. Calderwood. "Identification of Virulence Genes in a Pathogenic Strain of Pseudomonas aeruginosa by Representational Difference Analysis." Journal of Bacteriology 184, no. 4 (February 15, 2002): 952–61. http://dx.doi.org/10.1128/jb.184.4.952-961.2002.

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ABSTRACT Pseudomonas aeruginosa is an opportunistic pathogen that may cause severe infections in humans and other vertebrates. In addition, a human clinical isolate of P. aeruginosa, strain PA14, also causes disease in a variety of nonvertebrate hosts, including plants, Caenorhabditis elegans, and the greater wax moth, Galleria mellonella. This has led to the development of a multihost pathogenesis system in which plants, nematodes, and insects have been used as adjuncts to animal models for the identification of P. aeruginosa virulence factors. Another approach to identifying virulence genes in bacteria is to take advantage of the natural differences in pathogenicity between isolates of the same species and to use a subtractive hybridization technique to recover relevant genomic differences. The sequenced strain of P. aeruginosa, strain PAO1, has substantial differences in virulence from strain PA14 in several of the multihost models of pathogenicity, and we have utilized the technique of representational difference analysis (RDA) to directly identify genomic differences between P. aeruginosa strains PA14 and PAO1. We have found that the pilC, pilA, and uvrD genes in strain PA14 differ substantially from their counterparts in strain PAO1. In addition, we have recovered a gene homologous to the ybtQ gene from Yersinia, which is specifically present in strain PA14 but absent in strain PAO1. Mutation of the ybtQ homolog in P. aeruginosa strain PA14 significantly attenuates the virulence of this strain in both G. mellonella and a burned mouse model of sepsis to levels comparable to those seen with PAO1. This suggests that the increased virulence of P. aeruginosa strain PA14 compared to PAO1 may relate to specific genomic differences identifiable by RDA.

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Srichaisupakit, Akkaraphol, Peechanika Chopjitt, and Anusak Kerdsin. "Characterization of N4-like Pseudomonas Phage vB_Pae-PA14 Isolated from Seawater Sampled in Thailand." Journal of Pure and Applied Microbiology 15, no. 4 (November 22, 2021): 2347–57. http://dx.doi.org/10.22207/jpam.15.4.59.

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Bacteriophage, a predator virus of bacteria, is an abundant biological entity in the biosphere. With ultimate applications in medicine and biotechnology, new phages are extensively being isolated and characterized. The objective of the present study was to characterize lytic bacteriophage vB_Pae-PA14 infecting Pseudomonas aeruginosa ATCC 27853 that was isolated from seawater in Thailand. vB_Pae-PA14 was subjected to whole genome phylogenetic analysis, host range test, biofilm test and characterization. Results showed that the phage belonged to a group of N4-like viruses, could infect P. aeruginosa isolates including carbapenem-resistant P. aeruginosa. The burst size of vB_Pae-PA14 was 86 plaque-forming unit/infected cells. Also, the phage showed a greater ability to control planktonic P. aeruginosa cells than the biofilm cells. Phage could withstand physical stresses especially the high salt concentration. In brief, lytic bacteriophage vB_Pae-PA14 infecting P. aeruginosa was isolated and characterized, which might be useful in further bacteriophage lytic applications.

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Jander, Georg, Laurence G. Rahme, and Frederick M. Ausubel. "Positive Correlation between Virulence ofPseudomonas aeruginosa Mutants in Mice and Insects." Journal of Bacteriology 182, no. 13 (July 1, 2000): 3843–45. http://dx.doi.org/10.1128/jb.182.13.3843-3845.2000.

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ABSTRACT Strain PA14, a human clinical isolate of Pseudomonas aeruginosa, is pathogenic in mice and insects (Galleria mellonella). Analysis of 32 different PA14 mutants in these two hosts showed a novel positive correlation in the virulence patterns. Thus, G. mellonella is a good model system for identifying mammalian virulence factors of P. aeruginosa.

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Kukavica-Ibrulj, Irena, Alessandra Bragonzi, Moira Paroni, Craig Winstanley, François Sanschagrin, George A. O'Toole, and Roger C. Levesque. "In Vivo Growth of Pseudomonas aeruginosa Strains PAO1 and PA14 and the Hypervirulent Strain LESB58 in a Rat Model of Chronic Lung Infection." Journal of Bacteriology 190, no. 8 (December 14, 2007): 2804–13. http://dx.doi.org/10.1128/jb.01572-07.

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ABSTRACT Pseudomonas aeruginosa chronic lung infections are the major cause of morbidity and mortality in cystic fibrosis (CF) patients. The P. aeruginosa strains PAO1 and PA14 were compared with the Liverpool epidemic strain LESB58 to assess in vivo growth, infection kinetics, and bacterial persistence and localization within tissues in a rat model of chronic lung infection. The three P. aeruginosa strains demonstrated similar growth curves in vivo but differences in tissue distribution. The LESB58 strain persisted in the bronchial lumen, while the PAO1 and PA14 strains were found localized in the alveolar regions and grew as macrocolonies after day 7 postinfection. Bacterial strains were compared for swimming and twitching motility and for the production of biofilm. The P. aeruginosa LESB58 strain produced more biofilm than PAO1 and PA14. Competitive index (CI) analysis of PAO1, PA14, and LESB58 in vivo indicated CI values of 0.002, 0.0002, and 0.14 between PAO1-PA14, PAO1-LESB58, and LESB58-PA14, respectively. CI analysis comparing the in vivo growth of the PAO1 ΔPA5441 mutant and four PA14 surface attachment-defective (sad) mutants gave CI values 10 to 1,000 times lower in competitions with their respective wild-type strains PAO1 and PA14. P. aeruginosa strains studied in the rat model of chronic lung infection demonstrated similar in vivo growth but differences in virulence as shown with a competitive in vivo assay. These differences were further confirmed with biofilm and motility in vitro assays, where strain LESB58 produced more biofilm but had less capacity for motility than PAO1 and PA14.

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Al-Haidari, Rwaida A., Mona I. Shaaban, Sabrin R. M. Ibrahim, and Gamal A. Mohamed. "ANTI-QUORUM SENSING ACTIVITY OF SOME MEDICINAL PLANTS." African Journal of Traditional, Complementary and Alternative Medicines 13, no. 5 (August 12, 2016): 67–71. http://dx.doi.org/10.21010/ajtcam.v13i5.10.

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Background: Quorum sensing is the key regulator of virulence factors of Pseudomonas aeruginosa such as biofilm formation, motility, productions of proteases, hemolysin, pyocyanin, and toxins. Material and Methods: Quorum sensing inhibitory (OSI) effect of the alcohol extracts of 20 medicinal plants was evaluated by Chromobacterium violaceum reporter using agar cup diffusion method. The efficient QSI extracts were tested for their activity against biofilm synthesis, motility, and synthesis of pyocyanin from P. aeruginosa PA14 Results: The extracts of Citrus sinensis, Laurus nobilis, Elettaria cardamomum, Allium cepa, and Coriandrum sativum exhibited potent quorum quenching effect. On the other hand, Psidium guajava and Mentha longifolia extracts showed lower QSI activity. These extracts exhibited significant elimination of pyocyanin formation and biofilm development of Pseudomonas aeruginosa PA14. In addition, they significantly inhibited twitching and swimming motilities of P. aeruginosa PA14. Conclusion: This study illustrated for the first time the importance of C. sinensis, L. nobilis, E. cardamomum, A. cepa, and C. sativum as quorum sensing inhibitors and virulence suppressors of P. aeruginosa.

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Fu, Tse-Kai, Sim-Kun Ng, Yi-En Chen, Yuan-Chuan Lee, Fruzsina Demeter, Mihály Herczeg, Anikó Borbás, et al. "Rhamnose Binding Protein as an Anti-Bacterial Agent—Targeting Biofilm of Pseudomonas aeruginosa." Marine Drugs 17, no. 6 (June 14, 2019): 355. http://dx.doi.org/10.3390/md17060355.

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More than 80% of infectious bacteria form biofilm, which is a bacterial cell community surrounded by secreted polysaccharides, proteins and glycolipids. Such bacterial superstructure increases resistance to antimicrobials and host defenses. Thus, to control these biofilm-forming pathogenic bacteria requires antimicrobial agents with novel mechanisms or properties. Pseudomonas aeruginosa, a Gram-negative opportunistic nosocomial pathogen, is a model strain to study biofilm development and correlation between biofilm formation and infection. In this study, a recombinant hemolymph plasma lectin (rHPLOE) cloned from Taiwanese Tachypleus tridentatus was expressed in an Escherichia coli system. This rHPLOE was shown to have the following properties: (1) Binding to P. aeruginosa PA14 biofilm through a unique molecular interaction with rhamnose-containing moieties on bacteria, leading to reduction of extracellular di-rhamnolipid (a biofilm regulator); (2) decreasing downstream quorum sensing factors, and inhibiting biofilm formation; (3) dispersing the mature biofilm of P. aeruginosa PA14 to improve the efficacies of antibiotics; (4) reducing P. aeruginosa PA14 cytotoxicity to human lung epithelial cells in vitro and (5) inhibiting P. aeruginosa PA14 infection of zebrafish embryos in vivo. Taken together, rHPLOE serves as an anti-biofilm agent with a novel mechanism of recognizing rhamnose moieties in lipopolysaccharides, di-rhamnolipid and structural polysaccharides (Psl) in biofilms. Thus rHPLOE links glycan-recognition to novel anti-biofilm strategies against pathogenic bacteria.

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Wang, Yun, Suzanne E. Kern, and Dianne K. Newman. "Endogenous Phenazine Antibiotics Promote Anaerobic Survival of Pseudomonas aeruginosa via Extracellular Electron Transfer." Journal of Bacteriology 192, no. 1 (October 30, 2009): 365–69. http://dx.doi.org/10.1128/jb.01188-09.

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ABSTRACT Antibiotics are increasingly recognized as having other, important physiological functions for the cells that produce them. An example of this is the effect that phenazines have on signaling and community development for Pseudomonas aeruginosa (L. E. Dietrich, T. K. Teal, A. Price-Whelan, and D. K. Newman, Science 321:1203-1206, 2008). Here we show that phenazine-facilitated electron transfer to poised-potential electrodes promotes anaerobic survival but not growth of Pseudomonas aeruginosa PA14 under conditions of oxidant limitation. Other electron shuttles that are reduced but not made by PA14 do not facilitate survival, suggesting that the survival effect is specific to endogenous phenazines.

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Sass, Gabriele, Pallabi Shrestha, and David A. Stevens. "Pseudomonas aeruginosa Virulence Factors Support Voriconazole Effects on Aspergillus fumigatus." Pathogens 10, no. 5 (April 26, 2021): 519. http://dx.doi.org/10.3390/pathogens10050519.

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Pseudomonas aeruginosa and Aspergillus fumigatus are pathogens that are associated with deterioration of lung function, e.g., in persons with cystic fibrosis (CF). There is evidence that co-infections with these pathogens cause airway inflammation and aggravate pathology in CF lungs. Intermicrobial competition of P. aeruginosa and A. fumigatus has been described, but it is unknown how anti-fungal therapy is affected. The anti-fungal azole voriconazole (VCZ), supernatants of P. aeruginosa laboratory isolates PA14 or PAO1, or clinical isolate Pa10 independently inhibited biofilm metabolism of A. fumigatus isolates 10AF and AF13073. When VCZ and supernatants were combined at their IC50s, synergistic effects on A. fumigatus were found. Synergistic effects were no longer observed when P. aeruginosa supernatants were prepared in the presence of iron, or when P. aeruginosa mutants were lacking the ability to produce pyoverdine and pyochelin. Combination of pure P. aeruginosa products pyoverdine, pyochelin, and pyocyanin with VCZ showed synergistic anti-fungal effects. Combining VCZ with P. aeruginosa supernatants also improved its MIC and MFC against planktonic A. fumigatus. In summary, in the case of P. aeruginosa–A. fumigatus co-infections, it appeared that the P. aeruginosa co-infection facilitated therapy of the Aspergillus; lower concentrations of VCZ might be sufficient to control fungal growth.

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Budzik, Jonathan M., William A. Rosche, Arne Rietsch, and George A. O'Toole. "Isolation and Characterization of a Generalized Transducing Phage for Pseudomonas aeruginosa Strains PAO1 and PA14." Journal of Bacteriology 186, no. 10 (May 15, 2004): 3270–73. http://dx.doi.org/10.1128/jb.186.10.3270-3273.2004.

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ABSTRACT A temperate, type IV pilus-dependent, double-stranded DNA bacteriophage named DMS3 was isolated from a clinical strain of Pseudomonas aeruginosa. A clear-plaque variant of this bacteriophage was isolated. DMS3 is capable of mediating generalized transduction within and between P. aeruginosa strains PA14 and PAO1, thus providing a useful tool for the genetic analysis of P. aeruginosa.

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Van Alst, Nadine E., Melanie Wellington, Virginia L. Clark, Constantine G. Haidaris, and Barbara H. Iglewski. "Nitrite Reductase NirS Is Required for Type III Secretion System Expression and Virulence in the Human Monocyte Cell Line THP-1 by Pseudomonas aeruginosa." Infection and Immunity 77, no. 10 (August 3, 2009): 4446–54. http://dx.doi.org/10.1128/iai.00822-09.

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ABSTRACT The nitrate dissimilation pathway is important for anaerobic growth in Pseudomonas aeruginosa. In addition, this pathway contributes to P. aeruginosa virulence by using the nematode Caenorhabditis elegans as a model host, as well as biofilm formation and motility. We used a set of nitrate dissimilation pathway mutants to evaluate the virulence of P. aeruginosa PA14 in a model of P. aeruginosa-phagocyte interaction by using the human monocytic cell line THP-1. Both membrane nitrate reductase and nitrite reductase enzyme complexes were important for cytotoxicity during the interaction of P. aeruginosa PA14 with THP-1 cells. Furthermore, deletion mutations in genes encoding membrane nitrate reductase (ΔnarGH) and nitrite reductase (ΔnirS) produced defects in the expression of type III secretion system (T3SS) components, extracellular protease, and elastase. Interestingly, exotoxin A expression was unaffected in these mutants. Addition of exogenous nitric oxide (NO)-generating compounds to ΔnirS mutant cultures restored the production of T3SS phospholipase ExoU, whereas nitrite addition had no effect. These data suggest that NO generated via nitrite reductase NirS contributes to the regulation of expression of selected virulence factors in P. aeruginosa PA14.

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Kim, Han-Shin, and Hee-Deung Park. "Ginger Extract Inhibits Biofilm Formation by Pseudomonas aeruginosa PA14." PLoS ONE 8, no. 9 (September 27, 2013): e76106. http://dx.doi.org/10.1371/journal.pone.0076106.

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Rodríguez-Rojas, Alexandro, and Jesús Blázquez. "The Pseudomonas aeruginosa pfpI Gene Plays an Antimutator Role and Provides General Stress Protection." Journal of Bacteriology 191, no. 3 (November 21, 2000): 844–50. http://dx.doi.org/10.1128/jb.01081-08.

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ABSTRACT Hypermutator Pseudomonas aeruginosa strains, characterized by an increased spontaneous-mutation rate, are found at high frequencies in chronic lung infections. Hypermutability is associated with the loss of antimutator genes related to DNA repair or damage avoidance systems. Only a few antimutator genes have been described in P. aeruginosa, although there is some evidence that additional genes may be involved in naturally occurring hypermutability. In order to find new P. aeruginosa antimutator genes, we constructed and screened a library of random insertions in the PA14 strain. Some previously described P. aeruginosa and/or Escherichia coli antimutator genes, such as mutS, mutL, uvrD, mutT, ung, and mutY, were detected, indicating a good coverage of our insertional library. One additional mutant contained an insertion in the P. aeruginosa PA14-04650 (pfpI) gene, putatively encoding a member of the DJ-1/ThiJ/PfpI superfamily, which includes chaperones, peptidases, and the Parkinson's disease protein DJ-1a. The pfpI-defective mutants in both PAO1 and PA14 showed higher spontaneous mutation rates than the wild-type strains, suggesting that PfpI plays a key role in DNA protection under nonstress conditions. Moreover, the inactivation of pfpI resulted in a dramatic increase in the H2O2-induced mutant frequency. Global transcription studies showed the induction of bacteriophage Pf1 genes and the repression of genes related to iron metabolism, suggesting that the increased spontaneous-mutant frequency may be due to reduced protection against the basal level of reactive oxygen species. Finally, pfpI mutants are more sensitive to different types of stress and are affected in biofilm formation.

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Muller, Michael, and Neil D. Merrett. "Pyocyanin Production by Pseudomonas aeruginosa Confers Resistance to Ionic Silver." Antimicrobial Agents and Chemotherapy 58, no. 9 (July 7, 2014): 5492–99. http://dx.doi.org/10.1128/aac.03069-14.

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ABSTRACTSilver in its ionic form (Ag+), but not the bulk metal (Ag0), is toxic to microbial life forms and has been used for many years in the treatment of wound infections. The prevalence of bacterial resistance to silver is considered low due to the nonspecific nature of its toxicity. However, the recent increased use of silver as an antimicrobial agent for medical, consumer, and industrial products has raised concern that widespread silver resistance may emerge.Pseudomonas aeruginosais a common pathogen that produces pyocyanin, a redox toxin and a reductant for molecular oxygen and ferric (Fe3+) ions. The objective of this study was to determine whether pyocyanin reduces Ag+to Ag0, which may contribute to silver resistance due to lower bioavailability of the cation. Using surface plasmon resonance spectroscopy and scanning electron microscopy, pyocyanin was confirmed to be a reductant for Ag+, forming Ag0nanoparticles and reducing the bioavailability of free Ag+by >95% within minutes. Similarly, a pyocyanin-producing strain ofP. aeruginosa(PA14) reduced Ag+but not a pyocyanin-deficient (ΔphzM) strain of the bacterium. Challenge of each strain with Ag+(as AgNO3) gave MICs of 20 and 5 μg/ml for the PA14 and ΔphzMstrains, respectively. Removal of pyocyanin from the medium strain PA14 was grown in or its addition to the medium that ΔphzMmutant was grown in gave MICs of 5 and 20 μg/ml, respectively. Clinical isolates demonstrated similar pyocyanin-dependent resistance to Ag+. We conclude that pseudomonal silver resistance exists independently of previously recognized intracellular mechanisms and may be more prevalent than previously considered.

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Hao, Youai, Kathleen Murphy, Reggie Y. Lo, Cezar M. Khursigara, and Joseph S. Lam. "Single-Nucleotide Polymorphisms Found in themigAandwbpXGlycosyltransferase Genes Account for the Intrinsic Lipopolysaccharide Defects Exhibited by Pseudomonas aeruginosa PA14." Journal of Bacteriology 197, no. 17 (June 15, 2015): 2780–91. http://dx.doi.org/10.1128/jb.00337-15.

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ABSTRACTPseudomonas aeruginosaPA14 is widely used by researchers in many laboratories because of its enhanced virulence over strain PAO1 in a wide range of hosts. Although lipopolysaccharide (LPS) is an important virulence factor of allP. aeruginosastrains, the LPS of PA14 has not been characterized fully. A recent study showed that the structure of its O-specific antigen (OSA) belongs to serotype O19. We found that the OSA gene cluster of PA14 shares ∼99% identity with those of the O10/O19 group. These two serotypes share the same O-unit structure, except for anO-acetyl substitution in one of the sugars in O10. Here we showed that both PA14 and O19 LPS cross-reacted with the O10-specific monoclonal antibody MF76-2 in Western blots. Analysis by SDS-PAGE and silver staining showed that PA14 LPS exhibited modal chain lengths that were different from those of O19 LPS, in that only “very long” and “short” chain lengths were observed, while “medium” and “long” chain lengths were not detected. Two other novel observations included the lack of the uncapped core oligosaccharide epitope and of common polysaccharide antigen (CPA) LPS. The lack of the uncapped core oligosaccharide was caused by point mutations in the glycosyltransferase genemigA, while the CPA-negative phenotype was correlated with a single amino acid substitution, G20R, in the glycosyltransferase WbpX. Additionally, we showed that restoring CPA biosynthesis in PA14 significantly stimulated mature biofilm formation after 72 h, while outer membrane vesicle production was not affected.IMPORTANCEP. aeruginosaPA14 is a clinical isolate that has become an important reference strain used by many researchers worldwide. LPS of PA14 has not been characterized fully, and hence, confusion about its phenotype exists in the literature. In the present study, we set out to characterize the O-specific antigen (OSA), the common polysaccharide antigen (CPA), and the core oligosaccharide produced by PA14. We present evidence that PA14 produces an LPS consisting of “very-long-chain” and some “short-chain” OSA belonging to the O19 serotype but is devoid of CPA and the uncapped core oligosaccharide epitope. These intrinsic defects in PA14 LPS were due to single-nucleotide polymorphisms (SNPs) in the genes that encode glycosyltransferases in the corresponding biosynthesis pathways. Since sugars in CPA and the uncapped core are receptors for different bacteriocins and pyocins, the lack of CPA and an intact core may contribute to the increased virulence of PA14. Restoring CPA production in PA14 was found to stimulate mature biofilm formation.

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Friedman, Lisa, and Roberto Kolter. "Two Genetic Loci Produce Distinct Carbohydrate-Rich Structural Components of the Pseudomonas aeruginosa Biofilm Matrix." Journal of Bacteriology 186, no. 14 (July 15, 2004): 4457–65. http://dx.doi.org/10.1128/jb.186.14.4457-4465.2004.

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ABSTRACT Pseudomonas aeruginosa forms biofilms, which are cellular aggregates encased in an extracellular matrix. Molecular genetics studies of three common autoaggregative phenotypes, namely wrinkled colonies, pellicles, and solid-surface-associated biofilms, led to the identification of two loci, pel and psl, that are involved in the production of carbohydrate-rich components of the biofilm matrix. The pel gene cluster is involved in the production of a glucose-rich matrix material in P. aeruginosa strain PA14 (L. Friedman and R. Kolter, Mol. Microbiol. 51:675-690, 2004). Here we investigate the role of the pel gene cluster in P. aeruginosa strain ZK2870 and identify a second genetic locus, termed psl, involved in the production of a mannose-rich matrix material. The 11 predicted protein products of the psl genes are homologous to proteins involved in carbohydrate processing. P. aeruginosa is thus able to produce two distinct carbohydrate-rich matrix materials. Either carbohydrate-rich matrix component appears to be sufficient for mature biofilm formation, and at least one of them is required for mature biofilm formation in P. aeruginosa strains PA14 and ZK2870.

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Tetard, Alexandre, Susie Gaillot, Eline Dubois, Soumaya Aarras, Benoît Valot, Gilles Phan, Patrick Plésiat, and Catherine Llanes. "Exposure of Pseudomonas aeruginosa to Cinnamaldehyde Selects Multidrug Resistant Mutants." Antibiotics 11, no. 12 (December 10, 2022): 1790. http://dx.doi.org/10.3390/antibiotics11121790.

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Cinnamaldehyde (CNA), the main component of cinnamon essential oil, is one of the most active plant compounds against nosocomial pathogen Pseudomonas aeruginosa. Exposure of wild-type strain PA14 (MIC 700 µg/mL) for 5 to 10 days to fixed (900 µg/mL) or increasing (from 900 to 1400 µg/mL) concentrations of this natural antibacterial resulted in emergence of resistant mutants CNA-A1 to A3, and CNA-B1 to B7, respectively. Genome sequencing experiments showed that each of CNA-A1 to A3 mutants differed from PA14 by one SNP, and a slight increase in CNA resistance level (from 700 to 900 µg/mL). By comparison, mutants B1 to B7 were more resistant (up to 1100 µg/mL); each of them harbored multiple SNPs (from 24 to 39) likely as a consequence of alteration of DNA mismatch repair gene mutS. Of the ten mutants selected, eight contained mutations in gene nalC, which indirectly downregulates expression of the operon that codes for multidrug efflux system MexAB-OprM, and showed increased resistance (up to 16-fold versus PA14) to antibiotic molecules exported by the pump, including ß-lactams and fluoroquinolones. Of the six mutants with the highest CNA resistance, five were no longer motile because of alteration of genes flgJ, fliE and/or pilJ genes. Altogether, our data show that P. aeruginosa is able to adapt to strong electrophilic molecules such as CNA by upregulating its intrinsic efflux pump MexAB-OprM, and through less well-characterized pleiotropic changes. Whether multidrug-resistant mutants can emerge in patients using cinnamon essential oil as self-medication needs to be assessed further.

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Fung, Carina, Sharna Naughton, Lynne Turnbull, Pholawat Tingpej, Barbara Rose, Jonathan Arthur, Honghua Hu, et al. "Gene expression of Pseudomonas aeruginosa in a mucin-containing synthetic growth medium mimicking cystic fibrosis lung sputum." Journal of Medical Microbiology 59, no. 9 (September 1, 2010): 1089–100. http://dx.doi.org/10.1099/jmm.0.019984-0.

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Pseudomonas aeruginosa airway infection is the leading cause of morbidity and mortality in cystic fibrosis (CF) patients. Various in vitro models have been developed to study P. aeruginosa pathobiology in the CF lung. In this study we produced a modified artificial-sputum medium (ASMDM) more closely resembling CF sputum than previous models, and extended previous work by using strain PAO1 arrays to examine the global transcription profiles of P. aeruginosa strain UCBPP-PA14 under early exponential-phase and stationary-phase growth. In early exponential phase, 38/39 nutrition-related genes were upregulated in line with data from previous in vitro models using UCBPP-PA14. Additionally, 23 type III secretion system (T3SS) genes, several anaerobic respiration genes and 24 quorum-sensing (QS)-related genes were upregulated in ASMDM, suggesting enhanced virulence factor expression and priming for anaerobic growth and biofilm formation. Under stationary phase growth in ASMDM, macroscopic clumps resembling microcolonies were evident in UCBPP-PA14 and CF strains, and over 40 potentially important genes were differentially expressed relative to stationary-phase growth in Luria broth. Most notably, QS-related and T3SS genes were downregulated in ASMDM, and iron-acquisition and assimilatory nitrate reductase genes were upregulated, simulating the iron-depleted, microaerophilic/anaerobic environment of CF sputum. ASMDM thus appears to be highly suitable for gene expression studies of P. aeruginosa in CF.

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Saeki, Erika Kushikawa, Heloísa Moreira Martins, Larissa Ciappina de Camargo, Laís Anversa, Eliandro Reis Tavares, Sueli Fumie Yamada-Ogatta, Lucy Megumi Yamauchi Lioni, Renata Katsuko Takayama Kobayashi, and Gerson Nakazato. "Effect of Biogenic Silver Nanoparticles on the Quorum-Sensing System of Pseudomonas aeruginosa PAO1 and PA14." Microorganisms 10, no. 9 (August 30, 2022): 1755. http://dx.doi.org/10.3390/microorganisms10091755.

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The increase in multidrug-resistant microorganisms represents a global threat requiring the development novel strategies to fight bacterial infection. This study aimed to assess the effect of silver nanoparticles (bio-AgNPs) on bacterial growth, biofilm formation, production of virulence factors, and expression of genes related to the quorum-sensing (QS) system of P. aeruginosa PAO1 and PA14. Biofilm formation and virulence assays were performed with bio-AgNPs. RT-qPCR was carried out to determine the effect of bio-AgNPs on the QS regulatory genes lasI, lasR, rhlI, rhlR, pqsA, and mvfR. Bio-AgNPs had an MIC value of 62.50 μM, for both strains. Phenotypic and genotypic assays were carried out using sub-MIC values. Experimental results showed that treatment with sub-MICs of bio-AgNPs reduced (p < 0.05) the motility and rhamnolipids and elastase production in P. aeruginosa PAO1. In PA14, bio-AgNPs stimulated swarming and twitching motilities as well as biofilm formation and elastase and pyocyanin production. Bio-AgNP treatment increased (p < 0.05) the expression of QS genes in PAO1 and PA14. Despite the different phenotypic behaviors in both strains, both showed an increase in the expression of QS genes. Demonstrating that the bio-AgNPs acted in the induction of regulation. The possible mechanism underlying the action of bio-AgNPs involves the induction of the rhl and/or pqs system of PAO1 and of the las and/or pqs system of PA14. These results suggest that exposure to low concentrations of bio-AgNPs may promote the expression of QS regulatory genes in P. aeruginosa, consequently inducing the production of virulence factors such as elastase, pyocyanin, and biofilms.

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Phuong, Melissa S., Rafael E. Hernandez, and Subash Sad. "413. Differences in Inflammatory Mechanisms in Pseudomonas aeruginosa and Staphyloccoccus auereus Infections in Cystic Fibrosis." Open Forum Infectious Diseases 6, Supplement_2 (October 2019): S209. http://dx.doi.org/10.1093/ofid/ofz360.486.

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Abstract Background Chronic bacterial lung infections are the primary cause of morbidity and mortality in cystic fibrosis (CF). The most common CF pathogens, Pseudomonas aeruginosa (P. aeruginosa) or Staphylococcus aureus (S. aureus), are common commensal or environmental organisms that adapt to the CF lung. We sought to investigate whether adaptation from early lung colonizer to chronic pathogen alters the bacterial effects on host inflammation. Methods P. aeruginosa (n = 25) and S. aureus (n = 25) isolates from CF patients with early and chronic infections were acquired from Seattle Children’s CF. Environmental (n = 8) and clinical, non-CF P. aeruginosa (n = 8) isolates were obtained from the University of Ottawa. P. aeruginosa reference strain PA14 and PA14 transposon mutants for T3SS and flagellin were used to observe the relationship between cell death and cytokine production. We infected THP-1-derived macrophages (PMA differentiated) in vitro for 3 hours with various MOIs. We subsequently measured cell death of THP-1-derived macrophages using neutral red assay and cytokine production using ELISAs. Results Infections with PA14 mutants and non-CF P. aeruginosa isolates demonstrated that rapid cell death of THP-1-derived macrophages caused a reduction in cytokine production relative to strains that did not cause as much cell death. At 10 MOI, early P. aeruginosa isolates from CF patients induced more THP-1-derived macrophage cell death compared with chronic isolates (P < 0.0001). Chronic P. aeruginosa isolates induced greater production of TNF, IL-8, and IL-6 (P < 0.01, P < 0.0001, and P < 0.0001, respectively) compared with early strains. No difference in IL-1β production was observed. When controlling for cell death between the two groups by using heat-killed bacteria, the only difference maintained was in TNF production (P < 0.01). Between early and chronic S. aureus isolates, the one difference observed was greater IL-8 production among early isolates (P < 0.01). Conclusion Chronic P. aeruginosa isolates from CF patients induce less cell death but more TNF, IL-8, and IL-6 production compared with early isolates. This suggests that P. aeruginosa producing chronic infections induce inflammatory signals that may contribute to increased morbidity among CF patients. Disclosures All authors: No reported disclosures.

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Gavric, Damir, and Petar Knezevic. "Filamentous Pseudomonas Phage Pf4 in the Context of Therapy-Inducibility, Infectivity, Lysogenic Conversion, and Potential Application." Viruses 14, no. 6 (June 10, 2022): 1261. http://dx.doi.org/10.3390/v14061261.

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More than 20% of all Pseudomonas aeruginosa are infected with Pf4-related filamentous phage and although their role in virulence of P. aeruginosa strain PAO1 is well documented, its properties related to therapy are not elucidated in detail. The aim of this study was to determine how phage and antibiotic therapy induce Pf4, whether the released virions can infect other strains and how the phage influences the phenotype of new hosts. The subinhibitory concentrations of ciprofloxacin and mitomycin C increased Pf4 production for more than 50% during the first and sixth hour of exposure, respectively, while mutants appearing after infection with obligatory lytic phage at low MOI produced Pf4 more than four times after 12–24 h of treatment. This indicates that production of Pf4 is enhanced during therapy with these agents. The released virions can infect new P. aeruginosa strains, as confirmed for models UCBPP-PA14 (PA14) and LESB58, existing both episomally and in a form of a prophage, as confirmed by PCR, RFLP, and sequencing. The differences in properties of Pf4-infected, and uninfected PA14 and LESB58 strains were obvious, as infection with Pf4 significantly decreased cell autoaggregation, pyoverdine, and pyocyanin production, while significantly increased swimming motility and biofilm production in both strains. In addition, in strain PA14, Pf4 increased cell surface hydrophobicity and small colony variants’ appearance, but also decreased twitching and swarming motility. This indicates that released Pf4 during therapy can infect new strains and cause lysogenic conversion. The infection with Pf4 increased LESB58 sensitivity to ciprofloxacin, gentamicin, ceftazidime, tetracycline, and streptomycin, and PA14 to ciprofloxacin and ceftazidime. Moreover, the Pf4-infected LESB58 was re-sensitized to ceftazidime and tetracycline, with changes from resistant to intermediate resistant and sensitive, respectively. The obtained results open a new field in phage therapy—treatment with selected filamentous phages in order to re-sensitize pathogenic bacteria to certain antibiotics. However, this approach should be considered with precautions, taking into account potential lysogenic conversion.

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Lau, Gee W., Boyan C. Goumnerov, Cynthia L. Walendziewicz, Jennifer Hewitson, Wenzhong Xiao, Shalina Mahajan-Miklos, Ronald G. Tompkins, Lizabeth A. Perkins, and Laurence G. Rahme. "The Drosophila melanogaster Toll Pathway Participates in Resistance to Infection by the Gram-Negative Human Pathogen Pseudomonas aeruginosa." Infection and Immunity 71, no. 7 (July 2003): 4059–66. http://dx.doi.org/10.1128/iai.71.7.4059-4066.2003.

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ABSTRACT Pseudomonas aeruginosa is a gram-negative pathogen that infects immunocompromised and cystic fibrosis patients. The molecular basis of the host-P. aeruginosa interaction and the effect of specific P. aeruginosa virulence factors on various components of the innate immunity pathways are largely unknown. We examine interactions between P. aeruginosa virulence factors and components of innate immunity response in the Drosophila melanogaster model system to reveal the importance of the Toll signaling pathway in resistance to infection by the P. aeruginosa human isolate PA14. Using the two PA14-isogenic mutants plcS and dsbA, we show that Drosophila loss-of-function mutants of Spatzle, the extracellular ligand of Toll, and Dorsal and Dif, two NF-κB-like transcription factors, allow increased P. aeruginosa infectivity within fly tissues. In contrast, a constitutively active Toll mutant and a loss-of-function mutant of Cactus, an IκB-like factor that inhibits the Toll signaling, reduce infectivity. Our finding that Dorsal activity is required to restrict P. aeruginosa infectivity in Drosophila provides direct in vivo evidence for Dorsal function in adult fly immunity. Additionally, our results provide the basis for future studies into interactions between P. aeruginosa virulence factors and components of the Toll signaling pathway, which is functionally conserved between flies and humans.

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Friedman, Lisa, and Roberto Kolter. "Genes involved in matrix formation in Pseudomonas aeruginosa PA14 biofilms." Molecular Microbiology 51, no. 3 (December 16, 2003): 675–90. http://dx.doi.org/10.1046/j.1365-2958.2003.03877.x.

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Ouidir, Tassadit, Frédérique Jarnier, Pascal Cosette, Thierry Jouenne, and Julie Hardouin. "Characterization of N-terminal protein modifications in Pseudomonas aeruginosa PA14." Journal of Proteomics 114 (January 2015): 214–25. http://dx.doi.org/10.1016/j.jprot.2014.11.006.

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Berger, Carola, and Miriam A. Rosenbaum. "Spontaneous quorum sensing mutation modulates electroactivity of Pseudomonas aeruginosa PA14." Bioelectrochemistry 117 (October 2017): 1–8. http://dx.doi.org/10.1016/j.bioelechem.2017.04.006.

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Depke, Tobias, Susanne Häussler, and Mark Brönstrup. "The Peptide Chain Release Factor Methyltransferase PrmC Influences the Pseudomonas aeruginosa PA14 Endo- and Exometabolome." Metabolites 10, no. 10 (October 18, 2020): 417. http://dx.doi.org/10.3390/metabo10100417.

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Pseudomonas aeruginosa is one of the most important nosocomial pathogens and understanding its virulence is the key to effective control of P. aeruginosa infections. The regulatory network governing virulence factor production in P. aeruginosa is exceptionally complex. Previous studies have shown that the peptide chain release factor methyltransferase PrmC plays an important role in bacterial pathogenicity. Yet, the underlying molecular mechanism is incompletely understood. In this study, we used untargeted liquid and gas chromatography coupled to mass spectrometry to characterise the metabolome of a prmC defective P. aeruginosa PA14 strain in comparison with the corresponding strain complemented with prmC in trans. The comprehensive metabolomics data provided new insight into the influence of prmC on virulence and metabolism. prmC deficiency had broad effects on the endo- and exometabolome of P. aeruginosa PA14, with a marked decrease of the levels of aromatic compounds accompanied by reduced precursor supply from the shikimate pathway. Furthermore, a pronounced decrease of phenazine production was observed as well as lower abundance of alkylquinolones. Unexpectedly, the metabolomics data showed no prmC-dependent effect on rhamnolipid production and an increase in pyochelin levels. A putative virulence biomarker identified in a previous study was significantly less abundant in the prmC deficient strain.

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Hendrickson, Erik L., Joulia Plotnikova, Shalina Mahajan-Miklos, Laurence G. Rahme, and Frederick M. Ausubel. "Differential Roles of the Pseudomonas aeruginosaPA14 rpoN Gene in Pathogenicity in Plants, Nematodes, Insects, and Mice." Journal of Bacteriology 183, no. 24 (December 15, 2001): 7126–34. http://dx.doi.org/10.1128/jb.183.24.7126-7134.2001.

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ABSTRACT We cloned the rpoN (ntrA, glnF) gene encoding the alternate sigma factor ς54 from the opportunistic multihost pathogen Pseudomonas aeruginosastrain PA14. A marker exchange protocol was used to construct the PA14rpoN insertional mutationrpoN::Genr. PA14rpoN::Genr synthesized reduced levels of pyocyanin and displayed a variety of phenotypes typical of rpoN mutants, including a lack of motility and the failure to grow on nitrate, glutamate, or histidine as the sole nitrogen source. Compared to wild-type PA14,rpoN::Genr was ca. 100-fold less virulent in a mouse thermal injury model and was significantly impaired in its ability to kill the nematode Caenorhabditis elegans. In an Arabidopsis thaliana leaf infectivity assay, althoughrpoN::Genr exhibited significantly reduced attachment to trichomes, stomata, and the epidermal cell surface, did not attach perpendicularly to or perforate mesophyll cell walls, and proliferated less rapidly in Arabidopsisleaves, it nevertheless elicited similar disease symptoms to wild-typeP. aeruginosa PA14 at later stages of infection.rpoN::Genr was not impaired in virulence in a Galleria mellonella (greater wax moth) pathogenicity model. These data indicate that rpoN does not regulate the expression of any genes that encode virulence factors universally required for P. aeruginosa pathogenicity in diverse hosts.

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Prithiviraj, B., H. P. Bais, T. Weir, B. Suresh, E. H. Najarro, B. V. Dayakar, H. P. Schweizer, and J. M. Vivanco. "Down Regulation of Virulence Factors of Pseudomonas aeruginosa by Salicylic Acid Attenuates Its Virulence on Arabidopsis thaliana and Caenorhabditis elegans." Infection and Immunity 73, no. 9 (September 2005): 5319–28. http://dx.doi.org/10.1128/iai.73.9.5319-5328.2005.

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ABSTRACT Salicylic acid (SA) is a phenolic metabolite produced by plants and is known to play an important role in several physiological processes, such as the induction of plant defense responses against pathogen attack. Here, using the Arabidopsis thaliana-Pseudomonas aeruginosa pathosystem, we provide evidence that SA acts directly on the pathogen, down regulating fitness and virulence factor production of the bacteria. Pseudomonas aeruginosa PA14 showed reduced attachment and biofilm formation on the roots of the Arabidopsis mutants lox2 and cpr5-2, which produce elevated amounts of SA, as well as on wild-type Arabidopsis plants primed with exogenous SA, a treatment known to enhance endogenous SA concentration. Salicylic acid at a concentration that did not inhibit PA14 growth was sufficient to significantly affect the ability of the bacteria to attach and form biofilm communities on abiotic surfaces. Furthermore, SA down regulated three known virulence factors of PA14: pyocyanin, protease, and elastase. Interestingly, P. aeruginosa produced more pyocyanin when infiltrated into leaves of the Arabidopsis transgenic line NahG, which accumulates less SA than wild-type plants. This finding suggests that endogenous SA plays a role in down regulating the synthesis and secretion of pyocyanin in vivo. To further test if SA directly affects the virulence of P. aeruginosa, we used the Caenorhabiditis elegans-P. aeruginosa infection model. The addition of SA to P. aeruginosa lawns significantly diminished the bacterium's ability to kill the worms, without affecting the accumulation of bacteria inside the nematodes' guts, suggesting that SA negatively affects factors that influence the virulence of P. aeruginosa. We employed microarray technology to identify SA target genes. These analyses showed that SA treatment affected expression of 331 genes. It selectively repressed transcription of exoproteins and other virulence factors, while it had no effect on expression of housekeeping genes. Our results indicate that in addition to its role as a signal molecule in plant defense responses, SA works as an anti-infective compound by affecting the physiology of P. aeruginosa and ultimately attenuating its virulence.

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Harrison, Ewan M., Melissa E. K. Carter, Shelley Luck, Hong-Yu Ou, Xinyi He, Zixin Deng, Chris O'Callaghan, Aras Kadioglu, and Kumar Rajakumar. "Pathogenicity Islands PAPI-1 and PAPI-2 Contribute Individually and Synergistically to the Virulence of Pseudomonas aeruginosa Strain PA14." Infection and Immunity 78, no. 4 (February 1, 2010): 1437–46. http://dx.doi.org/10.1128/iai.00621-09.

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ABSTRACT Pseudomonas aeruginosa is a leading cause of hospital-acquired pneumonia and severe chronic lung infections in cystic fibrosis patients. The reference strains PA14 and PAO1 have been studied extensively, revealing that PA14 is more virulent than PAO1 in diverse infection models. Among other factors, this may be due to two pathogenicity islands, PAPI-1 and PAPI-2, both present in PA14 but not in PAO1. We compared the global contributions to virulence of PAPI-1 and PAPI-2, rather than that of individual island-borne genes, using murine models of acute pneumonia and bacteremia. Three isogenic island-minus mutants (PAPI-1-minus, PAPI-2-minus, and PAPI-1-minus, PAPI-2-minus mutants) were compared with the wild-type parent strain PA14 and with PAO1. Our results showed that both islands contributed significantly to the virulence of PA14 in acute pneumonia and bacteremia models. However, in contrast to the results for the bacteremia model, where each island was found to contribute individually, loss of the 108-kb PAPI-1 island alone was insufficient to measurably attenuate the mutant in the acute pneumonia model. Nevertheless, the double mutant was substantially more attenuated, and exhibited a lesser degree of virulence, than even PAO1 in the acute pneumonia model. In particular, its ability to disseminate from the lungs to the bloodstream was markedly inhibited. We conclude that both PAPI-1 and PAPI-2 contribute directly and synergistically in a major way to the virulence of PA14, and we suggest that analysis of island-minus strains may be a more appropriate way than individual gene knockouts to assess the contributions to virulence of large, horizontally acquired segments of DNA.

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Vasseur, Perrine, Isabelle Vallet-Gely, Chantal Soscia, Stéphane Genin, and Alain Filloux. "The pel genes of the Pseudomonas aeruginosa PAK strain are involved at early and late stages of biofilm formation." Microbiology 151, no. 3 (March 1, 2005): 985–97. http://dx.doi.org/10.1099/mic.0.27410-0.

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Pseudomonas aeruginosa is a Gram-negative bacterium associated with nosocomial infections and cystic fibrosis. Chronic bacterial infections are increasingly associated with the biofilm lifestyle in which microcolonies are embedded in an extracellular matrix. Screening procedures for identifying biofilm-deficient strains have allowed the characterization of several key determinants involved in this process. Biofilm-deficient P. aeruginosa PAK strains affected in a seven-gene cluster called pel were characterized. The pel genes encode proteins with similarity to components involved in polysaccharide biogenesis, of which PelF is a putative glycosyltransferase. PelG was also identified as a putative component of the polysaccharide transporter (PST) family. The pel genes were previously identified in the P. aeruginosa PA14 strain as required for the production of a glucose-rich matrix material involved in the formation of a thick pellicle and resistant biofilm. However, in PA14, the pel mutants have no clear phenotype in the initiation phase of attachment. It was shown that pel mutations in the PAK strain had little influence on biofilm initiation but, as in PA14, appeared to generate the least robust and mature biofilms. Strikingly, by constructing pel mutants in a non-piliated P. aeruginosa PAK strain, an unexpected effect of the pel mutation in the early phase of biofilm formation was discovered, since it was observed that these mutants were severely defective in the attachment process on solid surfaces. The pel gene cluster is conserved in other Gram-negative bacteria, and mutation in a Ralstonia solanacearum pelG homologue, ragG, led to an adherence defect.

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Wiegand, Irith, Alexandra K. Marr, Elena B. M. Breidenstein, Kristen N. Schurek, Patrick Taylor, and Robert E. W. Hancock. "Mutator Genes Giving Rise to Decreased Antibiotic Susceptibility in Pseudomonas aeruginosa." Antimicrobial Agents and Chemotherapy 52, no. 10 (July 28, 2008): 3810–13. http://dx.doi.org/10.1128/aac.00233-08.

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ABSTRACT Screening of the PA14 genomic transposon mutant library for resistance to ceftazidime, tobramycin, and ciprofloxacin led to the discovery of several mutants that appeared in more than one screen. Testing of the frequency of mutation to ciprofloxacin resistance revealed previously known mutator genes, including mutS and mutL, as well as mutators that have not yet been described for P. aeruginosa, including PA3958 and RadA (PA4609).

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Cole, Stephanie J., Angela R. Records, Mona W. Orr, Sara B. Linden, and Vincent T. Lee. "Catheter-Associated Urinary Tract Infection by Pseudomonas aeruginosa Is Mediated by Exopolysaccharide-Independent Biofilms." Infection and Immunity 82, no. 5 (March 4, 2014): 2048–58. http://dx.doi.org/10.1128/iai.01652-14.

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ABSTRACTPseudomonas aeruginosais an opportunistic human pathogen that is especially adept at forming surface-associated biofilms.P. aeruginosacauses catheter-associated urinary tract infections (CAUTIs) through biofilm formation on the surface of indwelling catheters.P. aeruginosaencodes three extracellular polysaccharides, PEL, PSL, and alginate, and utilizes the PEL and PSL polysaccharides to form biofilmsin vitro; however, the requirement of these polysaccharides duringin vivoinfections is not well understood. Here we show in a murine model of CAUTI that PAO1, a strain harboringpel,psl, andalggenes, and PA14, a strain harboringpelandalggenes, form biofilms on the implanted catheters. To determine the requirement of exopolysaccharide duringin vivobiofilm infections, we tested isogenic mutants lacking thepel,psl, andalgoperons and showed that PA14 mutants lacking these operons can successfully form biofilms on catheters in the CAUTI model. To determine the host factor(s) that induces the ΔpelDmutant to form biofilm, we tested mouse, human, and artificial urine and show that urine can induce biofilm formation by the PA14 ΔpelDmutant. By testing the major constituents of urine, we show that urea can induce apel-,psl-, andalg-independent biofilm. Thesepel-,psl-, andalg-independent biofilms are mediated by the release of extracellular DNA. Treatment of biofilms formed in urea with DNase I reduced the biofilm, indicating that extracellular DNA supports biofilm formation. Our results indicate that the opportunistic pathogenP. aeruginosautilizes a distinct program to form biofilms that are independent of exopolysaccharides during CAUTI.

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Miyata, Sachiko, Monika Casey, Dara W. Frank, Frederick M. Ausubel, and Eliana Drenkard. "Use of the Galleria mellonella Caterpillar as a Model Host To Study the Role of the Type III Secretion System in Pseudomonas aeruginosa Pathogenesis." Infection and Immunity 71, no. 5 (May 2003): 2404–13. http://dx.doi.org/10.1128/iai.71.5.2404-2413.2003.

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ABSTRACT Nonvertebrate model hosts represent valuable tools for the study of host-pathogen interactions because they facilitate the identification of bacterial virulence factors and allow the discovery of novel components involved in host innate immune responses. In this report, we determined that the greater wax moth caterpillar Galleria mellonella is a convenient nonmammalian model host for study of the role of the type III secretion system (TTSS) in Pseudomonas aeruginosa pathogenesis. Based on the observation that a mutation in the TTSS pscD gene of P. aeruginosa strain PA14 resulted in a highly attenuated virulence phenotype in G. mellonella, we examined the roles of the four known effector proteins of P. aeruginosa (ExoS, ExoT, ExoU, and ExoY) in wax moth killing. We determined that in P. aeruginosa strain PA14, only ExoT and ExoU play a significant role in G. mellonella killing. Strain PA14 lacks the coding sequence for the ExoS effector protein and does not seem to express ExoY. Moreover, using ΔexoU ΔexoY, ΔexoT ΔexoY, and ΔexoT ΔexoU double mutants, we determined that individual translocation of either ExoT or ExoU is sufficient to obtain nearly wild-type levels of G. mellonella killing. On the other hand, data obtained with a ΔexoT ΔexoU ΔexoY triple mutant and a ΔpscD mutant suggested that additional, as-yet-unidentified P. aeruginosa components of type III secretion are involved in virulence in G. mellonella. A high level of correlation between the results obtained in the G. mellonella model and the results of cytopathology assays performed with a mammalian tissue culture system validated the use of G. mellonella for the study of the P. aeruginosa TTSS.

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Müsken, Mathias, Stefano Di Fiore, Andreas Dötsch, Rainer Fischer, and Susanne Häussler. "Genetic determinants of Pseudomonas aeruginosa biofilm establishment." Microbiology 156, no. 2 (February 1, 2010): 431–41. http://dx.doi.org/10.1099/mic.0.033290-0.

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The establishment of bacterial biofilms on surfaces is a complex process that requires various factors for each consecutive developmental step. Here we report the screening of the comprehensive Harvard Pseudomonas aeruginosa PA14 mutant library for mutants exhibiting an altered biofilm phenotype. We analysed the capability of all mutants to form biofilms at the bottom of a 96-well plate by the use of an automated confocal laser-scanning microscope and found 394 and 285 genetic determinants of reduced and enhanced biofilm production, respectively. Overall, 67 % of the identified mutants were affected within genes encoding hypothetical proteins, indicating that novel developmental pathways are likely to be dissected in the future. Nevertheless, a common theme that emerged from the analysis of the genes with a predicted function is that the establishment of a biofilm requires regulatory components that are involved in survival under microaerophilic growth conditions, arginine metabolism, alkyl-quinolone signalling, pH homeostasis and the DNA repair system.

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Yeung, Amy T. Y., Ellen C. W. Torfs, Farzad Jamshidi, Manjeet Bains, Irith Wiegand, Robert E. W. Hancock, and Joerg Overhage. "Swarming of Pseudomonas aeruginosa Is Controlled by a Broad Spectrum of Transcriptional Regulators, Including MetR." Journal of Bacteriology 191, no. 18 (July 10, 2009): 5592–602. http://dx.doi.org/10.1128/jb.00157-09.

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ABSTRACT Pseudomonas aeruginosa exhibits swarming motility on semisolid surfaces (0.5 to 0.7% agar). Swarming is a more than just a form of locomotion and represents a complex adaptation resulting in changes in virulence gene expression and antibiotic resistance. In this study, we used a comprehensive P. aeruginosa PA14 transposon mutant library to investigate how the complex swarming adaptation process is regulated. A total of 233 P. aeruginosa PA14 transposon mutants were verified to have alterations in swarming motility. The swarming-associated genes functioned not only in flagellar or type IV pilus biosynthesis but also in processes as diverse as transport, secretion, and metabolism. Thirty-three swarming-deficient and two hyperswarming mutants had transposon insertions in transcriptional regulator genes, including genes encoding two-component sensors and response regulators; 27 of these insertions were newly identified. Of the 25 regulatory mutants whose swarming motility was highly impaired (79 to 97%), only 1 (a PA1458 mutant) had a major defect in swimming, suggesting that this regulator might influence flagellar synthesis or function. Twitching motility, which requires type IV pili, was strongly affected in only two regulatory mutants (pilH and PA2571 mutants) and was moderately affected in three other mutants (algR, ntrB, and nosR mutants). Microarray analyses were performed to compare the gene expression profile of a swarming-deficient PA3587 mutant to that of the wild-type PA14 strain under swarming conditions. PA3587 showed 63% homology to metR, which encodes a regulator of methionine biosynthesis in Escherichia coli. The observed dysregulation in the metR mutant of nine different genes required for swarming motility provided a possible explanation for the swarming-deficient phenotype of this mutant.

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Price-Whelan, Alexa, Lars E. P. Dietrich, and Dianne K. Newman. "Pyocyanin Alters Redox Homeostasis and Carbon Flux through Central Metabolic Pathways in Pseudomonas aeruginosa PA14." Journal of Bacteriology 189, no. 17 (May 25, 2007): 6372–81. http://dx.doi.org/10.1128/jb.00505-07.

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ABSTRACT The opportunistic pathogen Pseudomonas aeruginosa produces colorful, redox-active antibiotics called phenazines. Excretion of pyocyanin, the best-studied natural phenazine, is responsible for the bluish tint of sputum and pus associated with P. aeruginosa infections in humans. Although the toxicity of pyocyanin for other bacteria, as well as its role in eukaryotic infection, has been studied extensively, the physiological relevance of pyocyanin metabolism for the producing organism is not well understood. Pyocyanin reduction by P. aeruginosa PA14 is readily observed in standing liquid cultures that have consumed all of the oxygen in the medium. We investigated the physiological consequences of pyocyanin reduction by assaying intracellular concentrations of NADH and NAD+ in the wild-type strain and a mutant defective in phenazine production. We found that the mutant accumulated more NADH in stationary phase than the wild type. This increased accumulation correlated with a decrease in oxygen availability and was relieved by the addition of nitrate. Pyocyanin addition to a phenazine-null mutant also decreased intracellular NADH levels, suggesting that pyocyanin reduction facilitates redox balancing in the absence of other electron acceptors. Analysis of extracellular organic acids revealed that pyocyanin stimulated stationary-phase pyruvate excretion in P. aeruginosa PA14, indicating that pyocyanin may also influence the intracellular redox state by decreasing carbon flux through central metabolic pathways.

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Bankers-Fulbright, Jennifer, Alexander Sorum, Sandra Hinz, Anna Weitz, and Allison Zank. "Pseudomonas aeruginosa biological functions are inhibited by normal airway epithelial secretions: implications for cystic fibrosis (P3074)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 125.14. http://dx.doi.org/10.4049/jimmunol.190.supp.125.14.

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Abstract P. aeruginosa does not colonize healthy individuals, but it is the leading cause of death in patients with cystic fibrosis (CF). The ability of P. aeruginosa to readily colonize CF-lungs is at least partially related to alterations in airway secretions caused by the disease. In addition to being dehydrated, these secretions have reduced antimicrobial activity compared to that found in normal airways. Thus, we proposed that normal airway secretions contain one or more molecules that reduce P. aeruginosa virulence whereas CF airway secretions do not. To test this hypothesis in vitro, we collected apical secretions from polarized CFTR+ and CFTR- Calu-3 cell monolayers. We applied these secretions at various concentrations to the P. aeruginosa strain PA14 and examined the effect of the secretions on two key biological activities associated with P. aeruginosa virulence: motility and biofilm formation. Secretions from CFTR+ (“normal”) cells dose-dependently inhibited both PA14 flagellar motility and biofilm formation. However, secretions from CFTR- (“CF-like”) cells failed to inhibit either biological function. Our preliminary identification experiments suggest that the inhibitory agent(s) in the CFTR+ secretions is a heat-labile, large (>50 kDa) molecule, probably a protein. Thus, it is likely that normal epithelial secretions play a direct role in inhibiting P. aerugionsa virulence and that these secretions are dysfunctional in patients with CF.

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Zegans, Michael E., Daniel Wozniak, Edward Griffin, Christine M. Toutain-Kidd, John H. Hammond, Andrew Garfoot, and Joseph S. Lam. "Pseudomonas aeruginosa Exopolysaccharide Psl Promotes Resistance to the Biofilm Inhibitor Polysorbate 80." Antimicrobial Agents and Chemotherapy 56, no. 8 (May 14, 2012): 4112–22. http://dx.doi.org/10.1128/aac.00373-12.

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ABSTRACTPolysorbate 80 (PS80) is a nonionic surfactant and detergent that inhibits biofilm formation byPseudomonas aeruginosaat concentrations as low as 0.001% and is well tolerated in human tissues. However, certain clinical and laboratory strains (PAO1) ofP. aeruginosaare able to form biofilms in the presence of PS80. To better understand this resistance, we performed transposon mutagenesis with a PS80-resistant clinical isolate, PA738. This revealed that mutation ofalgCrendered PA738 sensitive to PS80 biofilm inhibition. AlgC contributes to the biosynthesis of the exopolysaccharides Psl and alginate, as well as lipopolysaccharide and rhamnolipid. Analysis of mutations downstream of AlgC in these biosynthetic pathways established that disruption of thepsloperon was sufficient to render the PA738 and PAO1 strains sensitive to PS80-mediated biofilm inhibition. Increased levels of Psl production in the presence of arabinose in a strain with an arabinose-induciblepslpromoter were correlated with increased biofilm formation in PS80. InP. aeruginosastrains MJK8 and ZK2870, known to produce both Pel and Psl, disruption of genes in thepslbut not thepeloperon conferred susceptibility to PS80-mediated biofilm inhibition. The laboratory strain PA14 does not produce Psl and does not form biofilms in PS80. However, when PA14 was transformed with a cosmid containing thepsloperon, it formed biofilms in the presence of PS80. Taken together, these data suggest that production of the exopolysaccharide Psl byP. aeruginosapromotes resistance to the biofilm inhibitor PS80.

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Weaver, Valerie B., and Roberto Kolter. "Burkholderia spp. Alter Pseudomonas aeruginosa Physiology through Iron Sequestration." Journal of Bacteriology 186, no. 8 (April 15, 2004): 2376–84. http://dx.doi.org/10.1128/jb.186.8.2376-2384.2004.

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ABSTRACT Pseudomonas aeruginosa and members of the Burkholderia cepacia complex often coexist in both the soil and the lungs of cystic fibrosis patients. To gain an understanding of how these different species affect each other's physiology when coexisting, we performed a screen to identify P. aeruginosa genes that are induced in the presence of Burkholderia. A random gene fusion library was constructed in P. aeruginosa PA14 by using a transposon containing a promoterless lacZ gene. Fusion strains were screened for their ability to be induced in the presence of Burkholderia strains in a cross-streak assay. Three fusion strains were induced specifically by Burkholderia species; all three had transposon insertions in genes known to be iron regulated. One of these fusion strains, containing a transposon insertion in gene PA4467, was used to characterize the inducing activity from Burkholderia. Biochemical and genetic evidence demonstrate that ornibactin, a siderophore produced by nearly all B. cepacia strains, can induce P. aeruginosa PA4467. Significantly, PA4467 is induced early in coculture with an ornibactin-producing but not an ornibactin-deficient B. cepacia strain, indicating that ornibactin can be produced by B. cepacia and detected by P. aeruginosa when the two species coexist.

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Caiazza, Nicky C., Judith H. Merritt, Kimberly M. Brothers, and George A. O'Toole. "Inverse Regulation of Biofilm Formation and Swarming Motility by Pseudomonas aeruginosa PA14." Journal of Bacteriology 189, no. 9 (March 2, 2007): 3603–12. http://dx.doi.org/10.1128/jb.01685-06.

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ABSTRACT We previously reported that SadB, a protein of unknown function, is required for an early step in biofilm formation by the opportunistic pathogen Pseudomonas aeruginosa. Here we report that a mutation in sadB also results in increased swarming compared to the wild-type strain. Our data are consistent with a model in which SadB inversely regulates biofilm formation and swarming motility via its ability both to modulate flagellar reversals in a viscosity-dependent fashion and to influence the production of the Pel exopolysaccharide. We also show that SadB is required to properly modulate flagellar reversal rates via chemotaxis cluster IV (CheIV cluster). Mutational analyses of two components of the CheIV cluster, the methyl-accepting chemotaxis protein PilJ and the PilJ demethylase ChpB, support a model wherein this chemotaxis cluster participates in the inverse regulation of biofilm formation and swarming motility. Epistasis analysis indicates that SadB functions upstream of the CheIV cluster. We propose that P. aeruginosa utilizes a SadB-dependent, chemotaxis-like regulatory pathway to inversely regulate two key surface behaviors, biofilm formation and swarming motility.

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Lee, Ji-Sun, Yun-Jeong Heo, Jeong K. Lee, and You-Hee Cho. "KatA, the Major Catalase, Is Critical for Osmoprotection and Virulence in Pseudomonas aeruginosa PA14." Infection and Immunity 73, no. 7 (July 2005): 4399–403. http://dx.doi.org/10.1128/iai.73.7.4399-4403.2005.

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ABSTRACT We demonstrate that among the three monofunctional catalases of Pseudomonas aeruginosa PA14, KatA and, to a lesser extent, KatB, but not KatE, are required for resistance to peroxide and osmotic stresses. KatA is crucial for adaptation to H2O2 stress and full virulence in both Drosophila melanogaster and mice. This dismantling of catalase roles represents a specialized catalytic system primarily involving KatA in responses to adverse environmental conditions.

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Liberati, N. T., J. M. Urbach, S. Miyata, D. G. Lee, E. Drenkard, G. Wu, J. Villanueva, T. Wei, and F. M. Ausubel. "An ordered, nonredundant library of Pseudomonas aeruginosa strain PA14 transposon insertion mutants." Proceedings of the National Academy of Sciences 103, no. 8 (February 13, 2006): 2833–38. http://dx.doi.org/10.1073/pnas.0511100103.

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Song, Lei, and XueHong Zhang. "Innovation for ascertaining genomic islands in PAO1 and PA14 of Pseudomonas aeruginosa." Chinese Science Bulletin 54, no. 21 (November 2009): 3991–99. http://dx.doi.org/10.1007/s11434-009-0598-0.

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Breidenstein, Elena B. M., Bhavjinder K. Khaira, Irith Wiegand, Joerg Overhage, and Robert E. W. Hancock. "Complex Ciprofloxacin Resistome Revealed by Screening a Pseudomonas aeruginosa Mutant Library for Altered Susceptibility." Antimicrobial Agents and Chemotherapy 52, no. 12 (September 29, 2008): 4486–91. http://dx.doi.org/10.1128/aac.00222-08.

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ABSTRACT Pseudomonas aeruginosa offers substantial therapeutic challenges due to its high intrinsic resistance to many antibiotics and its propensity to develop mutational and/or adaptive resistance. The PA14 comprehensive mutant library was screened for mutants exhibiting either two- to eightfold increased susceptibilities (revealing genes involved in intrinsic resistance) or decreased susceptibilities (mutational resistance) to the fluoroquinolone ciprofloxacin. Thirty-five and 79 mutants with increased and decreased susceptibilities, respectively, were identified, as confirmed by broth dilution.

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Giorgini, Giorgia, Gianmarco Mangiaterra, Nicholas Cedraro, Emiliano Laudadio, Giulia Sabbatini, Mattia Cantarini, Cristina Minnelli, et al. "Berberine Derivatives as Pseudomonas aeruginosa MexXY-OprM Inhibitors: Activity and In Silico Insights." Molecules 26, no. 21 (November 2, 2021): 6644. http://dx.doi.org/10.3390/molecules26216644.

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The natural alkaloid berberine has been demonstrated to inhibit the Pseudomonas aeruginosa multidrug efflux system MexXY-OprM, which is responsible for tobramycin extrusion by binding the inner membrane transporter MexY. To find a structure with improved inhibitory activity, we compared by molecular dynamics investigations the binding affinity of berberine and three aromatic substituents towards the three polymorphic sequences of MexY found in P. aeruginosa (PAO1, PA7, and PA14). The synergy of the combinations of berberine or berberine derivatives/tobramycin against the same strains was then evaluated by checkerboard and time-kill assays. The in silico analysis evidenced different binding modes depending on both the structure of the berberine derivative and the specific MexY polymorphism. In vitro assays showed an evident MIC reduction (32-fold and 16-fold, respectively) and a 2–3 log greater killing effect after 2 h of exposure to the combinations of 13-(2-methylbenzyl)- and 13-(4-methylbenzyl)-berberine with tobramycin against the tobramycin-resistant strain PA7, a milder synergy (a 4-fold MIC reduction) against PAO1 and PA14, and no synergy against the ΔmexXY strain K1525, confirming the MexY-specific binding and the computational results. These berberine derivatives could thus be considered new hit compounds to select more effective berberine substitutions and their common path of interaction with MexY as the starting point for the rational design of novel MexXY-OprM inhibitors.

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Kim, Seol-Hee, Shin-Young Park, Yun-Jeong Heo, and You-Hee Cho. "Drosophila melanogaster-Based Screening for Multihost Virulence Factors of Pseudomonas aeruginosa PA14 and Identification of a Virulence-Attenuating Factor, HudA." Infection and Immunity 76, no. 9 (June 30, 2008): 4152–62. http://dx.doi.org/10.1128/iai.01637-07.

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ABSTRACT Pseudomonas aeruginosa is an important opportunistic human pathogen that interacts with phylogenetically diverse nonmammalian hosts, including plants, nematodes, and insects. Here, we exploited the P. aeruginosa-induced killing of the fruit fly Drosophila melanogaster as an assay system to screen for virulence-attenuated mutants of P. aeruginosa PA14. Fifteen nonredundant mutants were isolated from 4,018 random transposon (TnphoA) insertion clones, and 13 out of them (86.7%) displayed significantly reduced virulence in a murine peritonitis model as well. The TnphoA insertion sites of the 15 mutants were determined; already known virulence genes (dsbA, pvdI, fhlB, pilF, and wspF) and new virulence genes such as PA0253 (hudR), PA0369, PA2077, PA0272, PA2113, PA2965 (fabF1), and PA2002 were identified; one insertion was located at the intergenic region between PA1928 and PA1929; and the other two insertions were located in the genes (PA14_35740 and PA14_36000) within a putative genomic island, indicating a potential pathogenicity island of PA14. Further characterization of hudR, a virulence gene which encodes a MarR/SlyA family transcription factor, revealed that elevated expression of PA0254 (hudA [homologous to UbiD]) was necessary and sufficient for the virulence attenuation of the hudR mutant. The HudR protein repressed the hudAR operon by directly binding to its upstream promoter region. Collectively, these results validate the relevance of the D. melanogaster model for the high-throughput identification of new virulence factors involved in the multihost pathogenesis of P. aeruginosa.

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Vasquez-Rifo, Alejandro, Emiliano P. Ricci, and Victor Ambros. "Pseudomonas aeruginosa cleaves the decoding center of Caenorhabditis elegans ribosomes." PLOS Biology 18, no. 12 (December 1, 2020): e3000969. http://dx.doi.org/10.1371/journal.pbio.3000969.

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Pathogens such as Pseudomonas aeruginosa advantageously modify animal host physiology, for example, by inhibiting host protein synthesis. Translational inhibition of insects and mammalian hosts by P. aeruginosa utilizes the well-known exotoxin A effector. However, for the infection of Caenorhabditis elegans by P. aeruginosa, the precise pathways and mechanism(s) of translational inhibition are not well understood. We found that upon exposure to P. aeruginosa PA14, C. elegans undergoes a rapid loss of intact ribosomes accompanied by the accumulation of ribosomes cleaved at helix 69 (H69) of the 26S ribosomal RNA (rRNA), a key part of ribosome decoding center. H69 cleavage is elicited by certain virulent P. aeruginosa isolates in a quorum sensing (QS)–dependent manner and independently of exotoxin A–mediated translational repression. H69 cleavage is antagonized by the 3 major host defense pathways defined by the pmk-1, fshr-1, and zip-2 genes. The level of H69 cleavage increases with the bacterial exposure time, and it is predominantly localized in the worm’s intestinal tissue. Genetic and genomic analysis suggests that H69 cleavage leads to the activation of the worm’s zip-2-mediated defense response pathway, consistent with translational inhibition. Taken together, our observations suggest that P. aeruginosa deploys a virulence mechanism to induce ribosome degradation and H69 cleavage of host ribosomes. In this manner, P. aeruginosa would impair host translation and block antibacterial responses.

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Kang, Yoon-Ho, Chong-Sung Park, and Myung-Soo Han. "Pseudomonas aeruginosa UCBPP-PA14 a useful bacterium capable of lysing Microcystis aeruginosa cells and degrading microcystins." Journal of Applied Phycology 24, no. 6 (February 29, 2012): 1517–25. http://dx.doi.org/10.1007/s10811-012-9812-6.

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Zegans, Michael E., Jeffrey C. Wagner, Kyle C. Cady, Daniel M. Murphy, John H. Hammond, and George A. O'Toole. "Interaction between Bacteriophage DMS3 and Host CRISPR Region Inhibits Group Behaviors of Pseudomonas aeruginosa." Journal of Bacteriology 191, no. 1 (October 24, 2008): 210–19. http://dx.doi.org/10.1128/jb.00797-08.

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ABSTRACT Bacteriophage infection has profound effects on bacterial biology. Clustered regular interspaced short palindromic repeats (CRISPRs) and cas (CRISPR-associated) genes are found in most archaea and many bacteria and have been reported to play a role in resistance to bacteriophage infection. We observed that lysogenic infection of Pseudomonas aeruginosa PA14 with bacteriophage DMS3 inhibits biofilm formation and swarming motility, both important bacterial group behaviors. This inhibition requires the CRISPR region in the host. Mutation or deletion of five of the six cas genes and one of the two CRISPRs in this region restored biofilm formation and swarming to DMS3 lysogenized strains. Our observations suggest a role for CRISPR regions in modifying the effects of lysogeny on P. aeruginosa.

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Strehmel, Janine, Anke Neidig, Michael Nusser, Robert Geffers, Gerald Brenner-Weiss, and Joerg Overhage. "Sensor Kinase PA4398 Modulates Swarming Motility and Biofilm Formation in Pseudomonas aeruginosa PA14." Applied and Environmental Microbiology 81, no. 4 (December 12, 2014): 1274–85. http://dx.doi.org/10.1128/aem.02832-14.

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ABSTRACTPseudomonas aeruginosais an opportunistic human pathogen that is able to sense and adapt to numerous environmental stimuli by the use of transcriptional regulators, including two-component regulatory systems. In this study, we demonstrate that the sensor kinase PA4398 is involved in the regulation of swarming motility and biofilm formation inP. aeruginosaPA14. A PA4398−mutant strain was considerably impaired in swarming motility, while biofilm formation was increased by approximately 2-fold. The PA4398−mutant showed no changes in growth rate, rhamnolipid synthesis, or the production of the Pel exopolysaccharide but exhibited levels of the intracellular second messenger cyclic dimeric GMP (c-di-GMP) 50% higher than those in wild-type cells. The role of PA4398 in gene regulation was investigated by comparing the PA4398−mutant to the wild-type strain by using microarray analysis, which demonstrated that 64 genes were up- or downregulated more than 1.5-fold (P< 0.05) under swarming conditions. In addition, more-sensitive real-time PCR studies were performed on genes known to be involved in c-di-GMP metabolism. Among the dysregulated genes were several involved in the synthesis and degradation of c-di-GMP or in the biosynthesis, transport, or function of the iron-scavenging siderophores pyoverdine and pyochelin, in agreement with the swarming phenotype observed. By analyzing additional mutants of selected pyoverdine- and pyochelin-related genes, we were able to show that not onlypvdQbut alsopvdR,fptA,pchA,pchD, andpchHare essential for the normal swarming behavior ofP. aeruginosaPA14 and may also contribute to the swarming-deficient phenotype of the PA4398−mutant in addition to elevated c-di-GMP levels.

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Cramer, N., S. Fischer, P. M. Losada, R. Hilker, S. Dethlefsen, M. Dorda, A. Munder, et al. "54 Intraclonal genome diversity of the major Pseudomonas aeruginosa clones C and PA14." Journal of Cystic Fibrosis 13 (June 2014): S60. http://dx.doi.org/10.1016/s1569-1993(14)60191-0.

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Journal articles on the topic 'Pseudomonas aeruginosa PA14'

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