scholarly journals Genome-Wide Identification of Pseudomonas aeruginosa Virulence-Related Genes Using a Caenorhabditis elegans Infection Model

2012 ◽  
Vol 8 (7) ◽  
pp. e1002813 ◽  
Author(s):  
Rhonda L. Feinbaum ◽  
Jonathan M. Urbach ◽  
Nicole T. Liberati ◽  
Slavica Djonovic ◽  
Allison Adonizio ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Caenorhabditis Elegans ◽  
Infection Model ◽  
Genome Wide

DI-ICR-FT-MS-based high-throughput deep metabotyping: a case study of the Caenorhabditis elegans–Pseudomonas aeruginosa infection model

2014 ◽  
Vol 407 (4) ◽  
pp. 1059-1073 ◽  
Author(s):  
Michael Witting ◽  
Marianna Lucio ◽  
Dimitrios Tziotis ◽  
Brigitte Wägele ◽  
Karsten Suhre ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Caenorhabditis Elegans ◽  
High Throughput ◽  
Infection Model ◽  
Pseudomonas Aeruginosa Infection

scholarly journals Feeding behaviour of Caenorhabditis elegans is an indicator of Pseudomonas aeruginosa PAO1 virulence

2014 ◽  
Author(s):  
Shawn Lewenza ◽  
Laetitia Charron-Mazenod ◽  
Lauriane Giroux ◽  
Alexandra D Zamponi
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Caenorhabditis Elegans ◽  
Feeding Behaviour ◽  
Food Sources ◽  
Infection Model ◽  
Bacterial Strains ◽  
Type Iii Effectors ◽  
Type Iii ◽  
C Elegans ◽  
Transposon Mutants

Caenorhabditis elegans is commonly used as an infection model for pathogenesis studies in Pseudomonas aeruginosa. While the standard virulence assays rely on the slow and fast killing or paralysis of nematodes, here we developed a behaviour assay to monitor the preferred bacterial food sources of C. elegans. The type III secretion system is a well-conserved virulence trait that is not required for slow or fast killing of C. elegans. However, ΔexsE mutants that are competent for hypersecretion of ExoS, ExoT and ExoY effectors were avoided as food sources in binary assays. Conversely, mutants lacking the secretion machinery or type III effectors were preferred food sources for PAO1. In binary feeding assays, both food sources were ingested and observed in the gastrointestinal tract, but non-preferred food sources were ultimately avoided. Next we developed a high throughput feeding behaviour assay to test a library of 2370 transposon mutants in order to identify preferred food sources. After primary and secondary screens, 37 mutants were identified as preferred food sources, which included mutations in many known virulence genes and that showed reduced virulence in the slow killing assay. We propose that C. elegans feeding behaviour can be used as a sensitive indicator of virulence for bacterial strains that have moderate worm killing activity.

scholarly journals Cephalosporins target quorum sensing and suppress virulence of Pseudomonas aeruginosa in Caenorhabditis elegans infection model

2020 ◽  
Author(s):  
Lokender Kumar ◽  
Nathanael Brenner ◽  
John Brice ◽  
Judith Klein-Seetharaman ◽  
Susanta K. Sarkar
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Caenorhabditis Elegans ◽  
Quorum Sensing ◽  
Virulence Factors ◽  
Biofilm Formation ◽  
Host Cells ◽  
Infection Model ◽  
Host Immune System ◽  
Bacterial Cells

ABSTRACTPseudomonas aeruginosa utilizes a chemical social networking system referred to as quorum sensing (QS) to strategically co-ordinate the expression of virulence factors and biofilm formation. Virulence attributes damage the host cells, impair the host immune system, and protect bacterial cells from antibiotic attack. Thus, anti-QS agents may act as novel anti-infective therapeutics to treat P. aeruginosa infections. The present study was performed to evaluate the anti-QS, anti-biofilm, and anti-virulence activity of β-lactam antibiotics (carbapenems and cephalosporins) against P. aeruginosa. The anti-QS activity was quantified using Chromobacterium violaceum CV026 as a QS reporter strain. Our results showed that cephalosporins including cefepime (CP), ceftazidime (CF), and ceftriaxone (CT) exhibited potent anti-QS and anti-virulence activities against P. aeruginosa PAO1. These antibiotics significantly impaired motility phenotypes, decreased pyocyanin production, and reduced the biofilm formation by P. aeruginosa PAO1. In the present study, we studied isogenic QS mutants of PAO1: ΔLasR, ΔRhlR, ΔPqsA, and ΔPqsR and found that the levels of virulence factors of antibiotic-treated PAO1 were comparable to QS mutant strains. Molecular docking predicted high binding affinities of cephalosporins for the ligand-binding pocket of QS receptors (CviR, LasR, and PqsR). In addition, our results showed that the anti-microbial activity of aminoglycosides increased in the presence of sub-inhibitory concentrations (sub-MICs) of CP against P. aeruginosa PAO1. Further, utilizing Caenorhabditis elegans as an animal model for the in vivo anti-virulence effects of antibiotics, cephalosporins showed a significant increase in C. elegans survival by suppressing virulence factor production in P. aeruginosa. Thus, our results indicate that cephalosporins might provide a viable anti-virulence therapy in the treatment of infections caused by multi-drug resistant P. aeruginosa.

scholarly journals Feeding behaviour of Caenorhabditis elegans is an indicator of Pseudomonas aeruginosa PAO1 virulence

2014 ◽  
Author(s):  
Shawn Lewenza ◽  
Laetitia Charron-Mazenod ◽  
Lauriane Giroux ◽  
Alexandra D Zamponi
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Caenorhabditis Elegans ◽  
Feeding Behaviour ◽  
Food Sources ◽  
Infection Model ◽  
Bacterial Strains ◽  
Type Iii Effectors ◽  
Type Iii ◽  
C Elegans ◽  
Transposon Mutants

Caenorhabditis elegans is commonly used as an infection model for pathogenesis studies in Pseudomonas aeruginosa. While the standard virulence assays rely on the slow and fast killing or paralysis of nematodes, here we developed a behaviour assay to monitor the preferred bacterial food sources of C. elegans. The type III secretion system is a well-conserved virulence trait that is not required for slow or fast killing of C. elegans. However, ΔexsE mutants that are competent for hypersecretion of ExoS, ExoT and ExoY effectors were avoided as food sources in binary assays. Conversely, mutants lacking the secretion machinery or type III effectors were preferred food sources for PAO1. In binary feeding assays, both food sources were ingested and observed in the gastrointestinal tract, but non-preferred food sources were ultimately avoided. Next we developed a high throughput feeding behaviour assay to test a library of 2370 transposon mutants in order to identify preferred food sources. After primary and secondary screens, 37 mutants were identified as preferred food sources, which included mutations in many known virulence genes and that showed reduced virulence in the slow killing assay. We propose that C. elegans feeding behaviour can be used as a sensitive indicator of virulence for bacterial strains that have moderate worm killing activity.

scholarly journals Quorum-Quenching Acylase Reduces the Virulence of Pseudomonas aeruginosa in a Caenorhabditis elegans Infection Model

2009 ◽  
Vol 53 (11) ◽  
pp. 4891-4897 ◽  
Author(s):  
Evelina Papaioannou ◽  
Mariana Wahjudi ◽  
Pol Nadal-Jimenez ◽  
Gudrun Koch ◽  
Rita Setroikromo ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Caenorhabditis Elegans ◽  
Type Strain ◽  
Wild Type Strain ◽  
Quorum Quenching ◽  
Homoserine Lactone ◽  
Infection Model ◽  
Wild Type ◽  
Strain Pao1

ABSTRACT The Pseudomonas aeruginosa PAO1 gene pvdQ encodes an acyl-homoserine lactone (AHL) acylase capable of degrading N-(3-oxododecanoyl)-l-homoserine lactone by cleaving the AHL amide. PvdQ has been proven to function as a quorum quencher in vitro in a number of phenotypic assays. To address the question of whether PvdQ also shows quorum-quenching properties in vivo, an infection model based on the nematode Caenorhabditis elegans was explored. In a fast-acting paralysis assay, strain PAO1(pMEpvdQ), which overproduces PvdQ, was shown to be less virulent than the wild-type strain. More than 75% of the nematodes exposed to PAO1(pMEpvdQ) survived and continued to grow when using this strain as a food source. Interestingly, in a slow-killing assay monitoring the survival of the nematodes throughout a 4-day course, strain PAO1-ΔpvdQ was shown to be more virulent than the wild-type strain, confirming the role of PvdQ as a virulence-reducing agent. It was observed that larval stage 1 (L1) to L3-stage larvae benefit much more from protection by PvdQ than L4 worms. Finally, purified PvdQ protein was added to C. elegans worms infected with wild-type PAO1, and this resulted in reduced pathogenicity and increased the life span of the nematodes. From our observations we can conclude that PvdQ might be a strong candidate for antibacterial therapy against Pseudomonas infections.

scholarly journals Disarming Pseudomonas aeruginosa Virulence Factor LasB by Leveraging a Caenorhabditis elegans Infection Model

2015 ◽  
Vol 22 (4) ◽  
pp. 483-491 ◽  
Author(s):  
Jie Zhu ◽  
Xiaoqing Cai ◽  
Tyler L. Harris ◽  
Major Gooyit ◽  
Malcolm Wood ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Caenorhabditis Elegans ◽  
Virulence Factor ◽  
Infection Model

scholarly journals Candida albicans SET3 Plays a Role in Early Biofilm Formation, Interaction With Pseudomonas aeruginosa and Virulence in Caenorhabditis elegans

2021 ◽  
Vol 11 ◽  
Author(s):  
Ruan Fourie ◽  
Jacobus Albertyn ◽  
Olihile Sebolai ◽  
Onele Gcilitshana ◽  
Carolina H. Pohl
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Candida Albicans ◽  
Caenorhabditis Elegans ◽  
Biofilm Formation ◽  
Transcriptional Analysis ◽  
Infection Model ◽  
Environmental Cues ◽  
Interspecies Interaction

The yeast Candida albicans exhibits multiple morphologies dependent on environmental cues. Candida albicans biofilms are frequently polymicrobial, enabling interspecies interaction through proximity and contact. The interaction between C. albicans and the bacterium, Pseudomonas aeruginosa, is antagonistic in vitro, with P. aeruginosa repressing the yeast-to-hyphal switch in C. albicans. Previous transcriptional analysis of C. albicans in polymicrobial biofilms with P. aeruginosa revealed upregulation of genes involved in regulation of morphology and biofilm formation, including SET3, a component of the Set3/Hos2 histone deacetylase complex (Set3C). This prompted the question regarding the involvement of SET3 in the interaction between C. albicans and P. aeruginosa, both in vitro and in vivo. We found that SET3 may influence early biofilm formation by C. albicans and the interaction between C. albicans and P. aeruginosa. In addition, although deletion of SET3 did not alter the morphology of C. albicans in the presence of P. aeruginosa, it did cause a reduction in virulence in a Caenorhabditis elegans infection model, even in the presence of P. aeruginosa.

scholarly journals Baicalin Represses Type Three Secretion System of Pseudomonas aeruginosa through PQS System

Molecules ◽  
2021 ◽  
Vol 26 (6) ◽  
pp. 1497
Author(s):  
Pansong Zhang ◽  
Qiao Guo ◽  
Zhihua Wei ◽  
Qin Yang ◽  
Zisheng Guo ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Virulence Factors ◽  
Mammalian Cells ◽  
Secretion System ◽  
Chinese Herbs ◽  
Infection Model ◽  
Lung Pathology ◽  
Promising Alternative ◽  
The Impact

Therapeutics that target the virulence of pathogens rather than their viability offer a promising alternative for treating infectious diseases and circumventing antibiotic resistance. In this study, we searched for anti-virulence compounds against Pseudomonas aeruginosa from Chinese herbs and investigated baicalin from Scutellariae radix as such an active anti-virulence compound. The effect of baicalin on a range of important virulence factors in P. aeruginosa was assessed using luxCDABE-based reporters and by phenotypical assays. The molecular mechanism of the virulence inhibition by baicalin was investigated using genetic approaches. The impact of baicalin on P. aeruginosa pathogenicity was evaluated by both in vitro assays and in vivo animal models. The results show that baicalin diminished a plenty of important virulence factors in P. aeruginosa, including the Type III secretion system (T3SS). Baicalin treatment reduced the cellular toxicity of P. aeruginosa on the mammalian cells and attenuated in vivo pathogenicity in a Drosophila melanogaster infection model. In a rat pulmonary infection model, baicalin significantly reduced the severity of lung pathology and accelerated lung bacterial clearance. The PqsR of the Pseudomonas quinolone signal (PQS) system was found to be required for baicalin’s impact on T3SS. These findings indicate that baicalin is a promising therapeutic candidate for treating P. aeruginosa infections.

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