Shotgun Proteomics Analyses of Pseudomonas Species Isolated from Fish Products Identification of Functional Networks and Virulence Factors
Ontology highlight
ABSTRACT:
INSTRUMENT(S): LTQ Orbitrap XL
ORGANISM(S): Pseudomonas Sp. (ncbitaxon:306)
SUBMITTER: 
Monica Carrera
PROVIDER: MSV000092812 | MassIVE |
SECONDARY ACCESSION(S): PXD045055
REPOSITORIES: MassIVE
Similar Datasets
Project description:Pseudomonas plecoglossicida is a facultative pathogen that is associated with diseases of multiple fish, mainly at 15-20 °C. Although fish disease caused by P. plecoglossicida has led to significant economic losses, the mechanisms of the temperature-dependent virulence are unclear. Here, we try to identify potential pathogenicity mechanisms and demonstrate the direct regulation of virulence factors by temperature with iTRAQ.
2018-11-22 | PXD009586 | Pride
Project description:Pseudomonas aeruginosa airway infection is the primary cause of death in Cystic Fibrosis (CF). During early infection P. aeruginosa produces multiple virulence factors, which cause acute pulmonary disease and are largely regulated by quorum sensing (QS) intercellular signalling networks. Longitudinal clinical studies have observed the loss, through adaptive mutation, of QS and QS-related virulence in late chronic infection. Although the mechanisms are not understood, infection with QS mutants has been linked to a worse outcome for CF patients. By comparing QS-active and QS-inactive P. aeruginosa CF isolates, we have identified novel virulence factors and pathways associated with QS disruption. In particular, we noted factors implicating increased intra-phagocyte survival. Our data present novel targets as candidates for future CF therapies. Some of these targets are already the subject of drug development programmes for the treatment of other bacterial pathogens and may provide cross-over benefit to the CF population. Refer to individual Series. This SuperSeries is composed of the following subset Series: GSE25128: Gene expression data from Pseudomonas aeruginosa strains isolated from cystic fibrosis lung infections GSE25129: Comparative genomic hybridisation data from Pseudomonas aeruginosa strains isolated from cystic fibrosis lung infections
2010-11-04 | E-GEOD-25130 | biostudies-arrayexpress
Project description:Quorum sensing is a communication strategy that bacteria use to collectively alter gene expression in response to cell density. Pathogens use quorum sensing systems to control activities vital to infection, such as the production of virulence factors and biofilm formation. The Pseudomonas virulence factor (pvf) gene cluster encodes a quorum sensing system (Pvf) that is present in over 500 strains of proteobacteria, including strains that infect a variety of plant and human hosts. We have shown that the Pvf quorum sensing system regulates the production of secreted proteins and small molecules in the insect pathogen Pseudomonas entomophila L48. Here, we identified genes that are likely regulated by Pvf using the model strain P. entomophila L48 which does not contain other known quorum sensing systems. Pvf regulated genes were identified through comparing the transcriptomes of wildtype P. entomophila and a pvf deletion mutant (ΔpvfA-D). We found that deletion of pvfA-D affected the expression of approximately 300 genes involved in virulence, the type VI secretion system, siderophore transport, and branched chain amino acid biosynthesis. Additionally, we identified seven putative biosynthetic gene clusters whose expression are reduced in ΔpvfA-D. Our results indicate that Pvf controls multiple virulence mechanisms in P. entomophila L48. Characterizing genes regulated by Pvf will aid understanding of host-pathogen interactions and development of anti-virulence strategies against P. entomophila and other pvf-containing strains.
2023-03-19 | GSE216056 | GEO
Project description:Pseudomonas syringae, a Gram-negative plant pathogen, infects more than 50 crops with its type III secretion system (T3SS) and causes severe economic losses around the world. Although the mechanisms of virulence-associated regulators of P. syringae T3SS have been studied for decades, the crosstalk and network underlying these regulators are still elusive. Previously, we have individually studied a group of T3SS regulators, including AefR, HrpS, and RhpRS. In the present study, we found 4 new T3SS regulator genes (envZ, ompR, tsiS and phoQ) via transposon-mediated mutagenesis. Two-component systems EnvZ and TsiS natively regulate T3SS. In order to uncover the crosstalk between 16 virulence-associated regulators, (including AefR, AlgU, CvsR, GacA, HrpL, HrpR, HrpS, MgrA, OmpR, PhoP, PilR, PsrA, RhpR, RpoN, TsiR and Vfr) in P. syringae, we mapped an intricate network named PSVnet (Pseudomonas syringae Virulence Regulatory Network) by combining differentially expression genes in RNA-seq and binding loci in ChIP-seq of all regulators.
2021-03-29 | GSE138204 | GEO
Project description:Pseudomonas aeruginosa airway infection is the primary cause of death in Cystic Fibrosis (CF). During early infection P. aeruginosa produces multiple virulence factors, which cause acute pulmonary disease and are largely regulated by quorum sensing (QS) intercellular signalling networks. Longitudinal clinical studies have observed the loss, through adaptive mutation, of QS and QS-related virulence in late chronic infection. Although the mechanisms are not understood, infection with QS mutants has been linked to a worse outcome for CF patients. By comparing QS-active and QS-inactive P. aeruginosa CF isolates, we have identified novel virulence factors and pathways associated with QS disruption. In particular, we noted factors implicating increased intra-phagocyte survival. Our data present novel targets as candidates for future CF therapies. Some of these targets are already the subject of drug development programmes for the treatment of other bacterial pathogens and may provide cross-over benefit to the CF population. This SuperSeries is composed of the SubSeries listed below.
2010-11-04 | GSE25130 | GEO
Project description:IntroductionThe Shewanella putrefaciens group are ubiquitous microorganisms recently isolated from different freshwater fish species and causing serious health disorders. The purpose of the study was to characterise isolates of the S. putrefaciens group with special emphasis on elucidating serological diversity and determining putative virulence factors.Material and methodsIsolates collected from freshwater fish (n = 44) and reference strains were used. The identification of bacteria was carried out using biochemical kits and 16S rRNA sequencing. Polyclonal antibodies were prepared against the S. putrefaciens group. The bacterium's susceptibility to antimicrobial agents, its enzymatic properties, and its adhesion ability to fish cell lines were also tested. Finally, selected isolates were used in challenge experiments in common carp and rainbow trout.ResultsExcluding six isolates undeterminable for species, the bacteria were classified to three species: S. putrefaciens, S. xiamenensis, and S. oneidensis, and showed some phenotypic diversity. Fourteen serological variants of the S. putrefaciens group were determined with the newly developed serotyping scheme.ConclusionSerodiversity may play an important role in the virulence of particular isolates. Further, S. putrefaciens group members adhere to epithelial cells and produce enzymes which may contribute to their virulence. Challenge tests confirmed the pathogenicity of the S. putrefaciens group for fish.
| S-EPMC6749743 | biostudies-literature
Project description:Pseudomonas aeruginosa and Staphylococcus aureus are often co-isolated in persistent infections. The goal of this study was to determine how secreted products that were identified in S. aureus supernatant affect gene expression in P. aeruginosa. Therefore, media control, the indicated products in media, or S. aureus supernatant was added to P. aeruginosa cultures at 25% total volume and gene expression was measured at 20 min and 2 h using RNA-seq. The individual products induced distinct pathways in P. aeruginosa. The products in combination recapitulated much of the differential gene expression seen in P. aeruginosa in response to S. aureus supernatant.
2022-05-18 | GSE186138 | GEO
Project description:Hypoxia is a feature of the microenvironment during P. aeruginosa infection in several disease states. We confirm that the pathogenicity of P. aeruginosa derived from sites of acute infection is higher than those derived from sites of chronic infection. Hypoxia attenuated the pathogenicity of acute but not chronic strains implicating a role for hypoxia in controlling virulence. Mass spectrometric analysis revealed reduced expression of multiple virulence factors in hypoxia including exotoxin A, alkaline protease and proteins important in the synthesis of pyoverdine. Inhibition of pyoverdine production by iron supplementation mimicked the effects of hypoxia. Finally, strains of P. aeruginosa which lacks a functional pseudomonas prolyl-hydroxylase domain containing protein (PPHD) do not respond to hypoxia implicating a possible role for PPHD as an oxygen-sensing determinant of pathogenicity. Understanding how hypoxia influences bacterial virulence will identify new targets for anti–infective therapy against P. aeruginosa.
2017-06-06 | PXD004421 | Pride
Project description:Pseudomonas aeruginosa is an opportunistic human pathogen, infecting immuno-compromised patients and causing persistent respiratory infections in people affected from cystic fibrosis. Pseudomonas strain Pseudomonas aeruginosa PA14 shows higher virulence than Pseudomonas aeruginosa PAO1 in a wide range of hosts including insects, nematodes and plants but the precise cause of this difference is not fully understood. Little is known about the host response upon infection with Pseudomonas and whether or not transcription is being affected as a host defense mechanism or altered in the benefit of the pathogen. In this context the social amoeba Dictyostelium discoideum has been described as a suitable host to study virulence of Pseudomonas and other opportunistic pathogens.
2008-07-09 | E-TABM-464 | biostudies-arrayexpress