Pseudomonas aeruginosa
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ABSTRACT:
PROVIDER: PRJNA1133673 | ENA |
REPOSITORIES: ENA
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Project description:Pseudomonas aeruginosa is an opportunistic pathogen which causes acute and chronic infections that are difficult to treat. Comparative genomic analysis has showed a great genome diversity among P. aeruginosa clinical strains and revealed important regulatory traits during chronic adaptation. While current investigation of epigenetics of P. aeruginosa is still lacking, understanding the epigenetic regulation may provide biomarkers for diagnosis and reveal important regulatory mechanisms. The present study focused on characterization of DNA methyltransferases (MTases) in a chronically adapted P. aeruginosa clinical strain TBCF10839. Single-molecule real-time sequencing (SMRT-seq) was used to characterize the methylome of TBCF. RCCANNNNNNNTGAR and TRGANNNNNNTGC were identified as target motifs of DNA MTases, M.PaeTBCFI and M.PaeTBCFII, respectively.
2023-07-22 | GSE209530 | GEO
Project description:Pseudomonas aeruginosa transcriptomes during biofilm dispersal in mouse chronic wounds
| PRJNA934328 | ENA
Project description:Bacterial infections of wounds are associated with poor healing and worse scarring. We sought to identify transcriptomic patterns associated with impaired healing of wounds infected with Klebsiella pneumoniae (K.p.) or Pseudomonas aeruginosa (P.a.) using a rabbit ear wound model. Wounds created on post-operative day (POD) 0 were infected on POD3, within the inflammatory phase of healing. On POD4 the infected wounds were harvested for microarray/transcriptome analysis. Other wounds with 24-hour infections were treated with topical antibiotic to promote biofilm formation and harvested on POD6 or POD12. On POD4 before antibiotic treatment, both wounds contained elevated transcripts that enriched predominantly into inflammation/infection-response pathways and functions characteristic of infiltrating leukocytes. But there were 5-fold more elevated transcripts in P.a.- than K.p.-infected wounds. Additionally, unique to P.a.-infected wounds, was a minor network of inflammation/infection-response molecules with predicted upstream regulation predominated by type I interferons. Also on POD4, Dnr-transcripts of both wounds were enriched into stress-response pathways such as EIF2 signaling. But there were 8-fold more Dnr-transcripts in P.a.- than K.p.-infected wounds, and many more of them enriched in the function, cell death, suggesting that resident dermal cells of P.a.-infected wounds failed to survive a more destructive P.a. infection. On POD6, following two days of antibiotic treatment, the biofilm-colonized wounds expressed magnitudes fewer inflammation and stress-response transcripts. However, a single regulatory network of P.a.-infected wounds was found to consist of Upr-transcripts enriching immune/infection-response functions predicted to be regulated by type I interferons, which was similar to the network unique to P.a.-infected wounds on POD4. On POD12, genes expressed by K.p.-infected wounds suggesting healing, while for P.a.-infected wounds they suggested stalled healing. The similarities and differences between the wound responses to these infections further define the molecular foundations of healing impaired by infections. Rabbit ear Wounds created on post-operative day (POD) 0 were infected with Klebsiella pneumoniae (K.p.) or Pseudomonas aeruginosa (P.a.) on POD3 and harvested on POD4 for RNA extraction. Other wounds with 24-hour infections were treated with topical antibiotic to promote biofilm formation and harvested on POD6 or POD12.
2014-01-01 | E-GEOD-51167 | biostudies-arrayexpress
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:Pseudomonas aeruginosa transcriptome adaptations from colonization to chronic infection of skin wounds
| PRJNA700644 | ENA
Project description:Pseudomonas aeruginosa RNA-seq and Tn-seq in burn and chronic wounds
| PRJNA231042 | ENA
Project description:Pseudomonas aeruginosa (PA) is an opportunistic pathogen frequently isolated from cutaneous chronic wounds. How PA, in the presence of oxidative stress (OS), colonizes chronic wounds and forms a biofilm is still unknown. The purpose of this study is to investigate the changes in gene expression seen when PA is challenged with the high levels of OS present in chronic wounds. We used a biofilm-forming PA strain isolated from the chronic wounds of our murine model (RPA) and performed a qPCR to obtain gene expression patterns as RPA developed a biofilm in vitro in the presence of high levels of OS, and then compared the findings in vivo, in our mouse model of chronic wounds. We found that the planktonic bacteria under OS conditions overex-pressed quorum sensing genes that are important for the bacteria to communicate with each other, antioxidant stress genes important to reduce OS in the microenvironment for survival, biofilm formation genes and virulence genes. Additionally, we performed RNAseq in vivo and identified the activation of novel genes/pathways of the Type VI Secretion System (T6SS) involved in RPA pathogenicity. In conclusion, RPA appears to survive the high OS microenvironment in chronic wounds and colonizes these wounds by turning on virulence, biofilm-forming and survival genes. These findings reveal pathways that may be promising targets for new therapies aimed at dis-rupting PA-containing biofilms immediately after debridement to facilitate the treatment of chronic human wounds.
2024-05-26 | GSE267862 | GEO
Project description:Pseudomonas aeruginosa is a common bacteria leading to exacerbations of chronic obstructive pulmonary disease (COPD) patients while this bacteria can be easily eradicated by the immune systems of healthy individuals. Human airway organoids derived from healthy individuals and COPD patients were infected with pseudomonas aeruginosa. This project aims (1) to understand the differences in gene expressions in healthy and COPD airway organoids during stable condition, without infection and (2) to investigate differential pathogenic mechanism (i.e. antimicrobial defense) of pseudomonoas aeruginosa infection in healthy and COPD populations. Three healthy donors and three COPD patients were included in this study and samples were collected with and without pseudomonas aeruginosa infection.
2022-11-10 | GSE201465 | GEO
Project description:Pseudomonas aeruginosa is a gram negative pathogen that infects acute wounds such as third degree skin injury and chronic wounds such as diabetic ulcers. Within infection sites, this pathogen exists in specific structures termed as biofilms. Biofilms contribute to enhanced resistance of microorganisms to the host defense and antibiotic treatments. Flagella, pilli and chaperon usher pathway (cup) fimbriae provide initial attachment to host tissue during biofilm development. pvcA-D operon codes for proteins which synthesize a secondary metabolite called paerucumarin. Paerucumarin is an isonitrile functionalized cumarin which is not extensively analyzed. We recently showed that paerucumarin enhances the expression of cup genes and biofilm development. We hypothesize that besides the cup genes pvcA-D operon regulates other P. aeruginosa genes. To test this hypothesis, we compared the transcriptome of P. aeruginosa strain MPAO1 with its pvcA mutant (MPAO1/pvcA). In comparison with MPAO1, 53 genes were differentially expressed in pvcA which included 19 up-regulated and 34 down-regulated genes. Functional characterization of differentially expressed genes indicated that 20 of these genes have been reported as iron regulated genes. Real time PCR confirmed these results and indicated that the expression of pvcAD operon is iron independent. However traditional chrome azurol S (CAS) iron binding assay showed that paerucumarin binds iron either within supernatants of MPAO1 or in solution. In addition, exogenously added paerucumarin enhances the expression of iron repressed genes pvdS and pvdA. Similarly, the level of pvdS gene expression in MPAO1?pvcA was significantly reduced as compared to MPAO1. Further analysis confirmed that paerucumarin binds iron in MPAO1 but does not deliver it inside the cell. The growth of a PAO1 double mutant strain (?pvdD?pchA), defective in iron scavenging systems, grown in iron deficient medium was restricted. However, the growth was restricted even further upon addition of exogenous paerucumarin to bacterial cultures. These results suggest that paerucumarin chelates iron but does not function as an iron scavenging system. 4 biological replicates of each strain were randomly paired
2014-01-01 | E-GEOD-45973 | biostudies-arrayexpress