E-GEOD-51043
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA219735
PROVIDER: E-GEOD-51043 | ExpressionAtlas | 2025-01-24
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-51043-analysis-methods.tsv | Tabular | |||
| E-GEOD-51043-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-51043-configuration.xml | Xml | |||
| E-GEOD-51043-percentile-ranks.tsv | Tabular | |||
| E-GEOD-51043.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 48 |
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Project description:Global impact of Salmonella type III secretion effector SteA on host cells
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Project description:SrfJ is an effector of the type III secretion systems of the Gram-negative intracellular pathogen Salmonella enterica serovar Typhimurium. To study the effects of this effector on global gene expression in host cells, we have expressed SrfJ on human HeLa cells through transient transfection. The comparison with HeLa cells transfected with a plasmid not expressing SrfJ, revealed a number of genes that are differentially expressed when SrfJ is present.
2023-05-17 | GSE215051 | GEO
Project description:SrfJ is an effector of the type III secretion systems of the Gram-negative intracellular pathogen Salmonella enterica serovar Typhimurium. To study the effects of this effector on global gene expression in host cells, we have infected murine RAW264.7 macrophages with two strains of Salmonella enterica serovar Typhimurium. The comparison between cells infected with the wild-type strain and cells infected with a srfJ mutant revealed a number of genes that are differentially expressed when SrfJ is present.
2023-05-17 | GSE215053 | GEO
Project description:Global expression profiling of airway epithelial cells infected with Pseudomonas aeruginosa and the rsmA mutant. Recent work in our laboratory investigated the impact of RsmA on a number of airway epithelial cell phenotypes including actin depolymerization, cytotoxicity and invasion. These cellular phenotypes were influenced by the positive effect of RsmA on the expression of the TTSS in P. aeruginosa (Mulcahy et al. 2006. Infect. Immun.). Pseudomonas aeruginosa is an important opportunistic pathogen which is capable of causing both acute and chronic infections in immunocompromised patients. Successful adaptation of the bacterium to its host environment relies on the ability of the organism to tightly regulate gene expression. RsmA, a small RNA-binding protein, controls the expression of a large number of virulence-related genes in P. aeruginosa, including those encoding the type III secretion system and associated effector proteins, with important consequences for epithelial cell morphology and cytotoxicity. In order to examine the influence of RsmA-regulated functions in the pathogen on gene expression in the host, we compared global expression profiles of airway epithelial cells in response to infection with P. aeruginosa PAO1 and an rsmA mutant. The RsmA-dependent response of host cells was characterized by significant changes in the global transcriptional pattern, including the increased expression of two Kruppel-like factors, KLF2 and KLF6. This increased expression was mediated by specific type III effector proteins. ExoS was required for the enhanced expression of KLF2, whereas both ExoS and ExoY were required for the enhanced expression of KLF6. Neither ExoT nor ExoU influenced the expression of the transcription factors. Additionally, the increased gene expression of KLF2 and KLF6 was associated with ExoS-mediated cytotoxicity. Therefore, this study identifies for the first time the human transcription factors KLF2 and KLF6 as targets of the P. aeruginosa type III exoenzymes S and Y, with potential importance in host cell death. Keywords: Expression profiling, Pseudomonas aeruginosa, microbial infection, airway epithelial cells, cystic fibrosis, exoenzymes, ExoS, ExoT, ExoU, ExoY, Kruppel-like factors, KLF2, KLF6
2006-09-15 | GSE4485 | GEO
Project description:Many Gram-negative pathogens use type III secretion systems to inject networks of effectors that subvert host cell processes. We modelled the robustness of such network using the mouse pathogen Citrobacter rodentium (encoding 31 effectors) through sequential deletions of effector genes, generating 100 distinct mutant combinations, which were tested in vivo. Counterintuitively, mutants lacking 19 unrelated effectors (CR14) or 10 immune-modulating effectors (CRi9) colonised and induced conserved molecular signatures of infection in intestinal epithelial cells. Specifically, CRi9 triggered heightened colonic secretion of TNF, IL-22, IL-17A and IFN-γ, while CR14 induced high-level secretion of IL-6 and GM-CSF with lower recruitment of myeloid cells. Yet, both CR14 and CRi9 induced sterile immunity. A machine learning model, trained on the mutant phenotypes and effector function, predicted an unprecedented combination of colonisation-failure effector mutations, which was validated experimentally. These results reveal the robustness and combinatorial plasticity of both the effector network and host immunity.
2022-04-06 | PXD018740 | Pride
Project description:Due to low numbers and poor accessibility of host cells that are targeted for effector delivery, the actual biological functions of most effectors remain elusive. Here, we developed a novel Isolation Nuclei TArgeted by Bacterial Effectors (INTABE) system, which facilitates selectively recovering nuclei of the cells in Arabidopsis thaliana plants that have received type-III effectors of pathogenic Xanthomonas bacteria. Using these nuclei as studying materials, we analysed changes in host gene expression and their correlation with changes in DNA methylation induced by Xanthomonas effector Outer Protein D (XopD).
2022-10-22 | E-MTAB-10281 | biostudies-arrayexpress
Project description:Injection of effectors via a type III secretion system (T3SS) is an infection strategy shared by many Gram-negative bacterial pathogens. While individual T3SS effectors are well characterized, their network-level organization and the distinction between core and accessory effectors remain incompletely understood. Here, we systematically dissect the T3SS effector network from Citrobacter rodentium (CR), identifying a subset of 12 accessory effectors that, while dispensable for colonization, significantly alter infection outcomes. A strain lacking these effectors (CRM12) remained virulent in susceptible hosts yet resulted in reduced epithelial barrier damage, inflammation and immune cell infiltration in resistant mouse hosts. Deep proteomic analysis specifically targeting CR-attached colonic epithelial cells revealed that, despite lacking 39% of its effector repertoire, infection with CRM12 results in similar changes to global protein expression as seen in mice infected with the wild-type strain, though key regulators of barrier disruption were differentially expressed. Using a host model with impaired barrier repair, we confirmed that accessory effectors shape infection dynamics without significantly impacting virulence. This study thus refines the concept of core and accessory effectors, providing a basis for further studies into effector-driven host adaptation.
2025-04-16 | PXD062886 | Pride
Project description:The bacterial type III secretion system (TTSS) is dedicated to directly effect host cell pathways by pathogens. In order to identify the key host responses of the various parts of the TTSS, we utilized expression profiling of a lung pneumocytes cell line, A549, exposed to various isogenic mutant strains of Pseudomonas aeruginosa PAK. We have devised a novel filtering method to isolate the key responses to the effector proteins as well as the translocation machinery. Individually, the effector proteins elicited host responses that were consistent with the known function of each, many of which either regulated, or are regulated by the cell cycle. However, our analysis has shown that the effector proteins elicit a distinct host expression pattern when present in combination, suggesting that these proteins function in synergy. Furthermore, the host transcriptional response to the translocation complex involved genes that are involved in remodeling of the plasma membrane, suggesting that the host cell is able to sense the protrusion of the TTSS machinery. This study shows that the individual components of the TTSS define an integrated system and that a systems biology approach is required to fully understand the complex interplay between pathogen and host.
2007-08-03 | E-GEOD-1469 | biostudies-arrayexpress
Project description:Previous work has shown that locus of enterocyte effacement (LEE)-encoded effector proteins such as Tir and Map can be exported via the type III secretion system (T3SS) of E. coli O157:H7. Additionally, a family of non-LEE encoded (Nle) effector proteins has been shown to be secreted from Citrobacter rodentium, homologues of which are located on the E. coli O157 chromosome. While, NleA has been shown to be secreted from pathogenic E. coli, the secretion of other Nle effector proteins has only been detected under induced conditions or using a mutated type III secretion system. We aimed to determine if nle gene expression is regulated co-ordinately with other LEE-encoded effectors. Using data generated from a combination of transcriptome arrays, we demonstrate that only nleA is expressed co-ordinately with the LEE effector genes. Secretion and expression of NleA is regulated directly or indirectly by ler, a key activator of LEE expression. Keywords: iMedia induction
2007-01-30 | GSE6296 | GEO
Project description:Salmonella enterica is an important foodborne pathogen that utilizes secreted effector proteins to manipulate host pathways to facilitate survival and dissemination. Different S. enterica serovars cause disease syndromes ranging from self-limited gastroenteritis to typhoid fever and vary in their repertoire of effectors. We leveraged this natural diversity to identify stm2585, here designated sarA (Salmonella anti-inflammatory response activator), as a Salmonella effector secreted primary by the SPI-2 type III secretion system. SarA is necessary and sufficient to induce STAT3 phosphorylation and IL-10 production, contributing to intracellular replication in vitro and bacterial load at systemic sites in mice. These results demonstrate that Salmonella has evolved effector mechanisms for regulating a host anti-inflammatory signaling pathway important in infection, autoimmunity, and cancer.
2018-06-01 | GSE104354 | GEO