Ontology highlight
ABSTRACT:
PROVIDER: PRJNA243386 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1175460_1.fastq.gz | Fastqsanger.gz | |||
| SRR1175460_2.fastq.gz | Fastqsanger.gz | |||
| SRR1175461_1.fastq.gz | Fastqsanger.gz | |||
| SRR1175461_2.fastq.gz | Fastqsanger.gz | |||
| SRR1175462_1.fastq.gz | Fastqsanger.gz |
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Project description:Complex in vivo RNA-seq analysis reveal reprogramming of Yersinia from virulent to persistent mode during infection [microarray II]
| PRJNA243387 | ENA
Project description:Complex in vivo RNA-seq analysis reveal reprogramming of Yersinia from virulent to persistent mode during infection [microarray I]
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Project description:Complex in vivo RNA-seq analysis reveal reprogramming of Yersinia from virulent to persistent mode during infection [RNA-seq]
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Project description:We recently found that Yersinia pseudotuberculosis can be used as a model of persistent bacterial infections. We performed in vivo RNA-seq of bacteria in small cecal tissue biopsies at early and persistent stages of infection to determine strategies associated with persistence. Comprehensive analysis of mixed RNA populations from infected tissues revealed that Y. pseudotuberculosis undergoes transcriptional reprogramming with drastic down-regulation of T3SS virulence genes during persistence when the pathogen resides within the cecum. At the persistent stage, the expression pattern in many respects resembles the pattern seen in vitro at 26oC, with for example up-regulation of flagellar genes and invA. These findings are expected to have impact on future rationales to identify suitable bacterial targets for new antibiotics. Other genes that are up-regulated during persistence are genes involved in anaerobiosis, chemotaxis, and protection against oxidative and acidic stress, which indicates the influence of different environmental cues. We found that the Crp/CsrA/RovA regulatory cascades influence the pattern of bacterial gene expression during persistence. Furthermore, arcA, fnr, frdA, and wrbA play critical roles in persistence. Our findings suggest a model for the life cycle of this enteropathogen with reprogramming from a virulent to an adapted phenotype capable of persisting and spreading by fecal shedding. Examination of Y. pseudotuberculosis expression in two mouse cecal tissue at early and at persistent infection. Also pure bacterial cultures two at 26C and two 37C. Additionally, the bacterial content of cecal tissue during infections and before infection were analyzed with read mapping on 16SMicrobial NCBI database with non-rRNA-depleted reads.
2014-12-05 | E-GEOD-55292 | biostudies-arrayexpress
Project description:We recently found that Yersinia pseudotuberculosis can be used as a model of persistent bacterial infections. We performed in vivo RNA-seq of bacteria in small cecal tissue biopsies at early and persistent stages of infection to determine strategies associated with persistence. Comprehensive analysis of mixed RNA populations from infected tissues revealed that Y. pseudotuberculosis undergoes transcriptional reprogramming with drastic down-regulation of T3SS virulence genes during persistence when the pathogen resides within the cecum. At the persistent stage, the expression pattern in many respects resembles the pattern seen in vitro at 26oC, with for example up-regulation of flagellar genes and invA. These findings are expected to have impact on future rationales to identify suitable bacterial targets for new antibiotics. Other genes that are up-regulated during persistence are genes involved in anaerobiosis, chemotaxis, and protection against oxidative and acidic stress, which indicates the influence of different environmental cues. We found that the Crp/CsrA/RovA regulatory cascades influence the pattern of bacterial gene expression during persistence. Furthermore, arcA, fnr, frdA, and wrbA play critical roles in persistence. Our findings suggest a model for the life cycle of this enteropathogen with reprogramming from a virulent to an adapted phenotype capable of persisting and spreading by fecal shedding.
2014-12-05 | GSE55292 | GEO
Project description:Pathogen invasion in plants is associated with transcriptional reprogramming. Enigmatically, plants induce similar transcriptome responses upon infection by virulent or avirulent pathogens. This renders the importance of transcriptional reprogramming for immunity obscure. Here, using RNA-seq, we generate time-series transcriptome data coupled with genetic perturbations to reveal temporal dynamics upon infection by virulent or avirulent strains of a bacterial pathogen, Pseudomonas syringae, in Arabidopsis thaliana. Fast and sustained transcriptional reprogramming occurs upon infection with avirulent strains while virulent strain infection leads to a slower response with comparable gene expression patterns and magnitudes. Importantly, transcriptome analysis of resistant and susceptible mutants responding to avirulent strains links delayed transcriptional reprogramming to compromised immunity. Taken together, our results pinpoint the early critical time window of transcriptional reprogramming for establishing effective immunity against the bacterial pathogen.
2017-12-12 | GSE88798 | GEO
Project description:RNA-sequencing was preformed from RNA isolated from bacteria infected with the bacteriophage. In order to reveal the phage-host interactions between φR1-37 and Yersinia enterocolitica throughout the phage infection cycle, both the transcriptomes were scrutinized during all the stages of infection.
2016-01-22 | GSE77068 | GEO
Project description:Gastric intestinal metaplasia (GIM) is an important precancerous lesion in intestinal-type gastric cancer, with persistent Helicobacter pylori (H. pylori) infection inducing the condition. In a previous study, we identified a new H. pylori virulence factor, SlyD. However, its mode of action between GIM was unknown. Our findings offer clues to reveal the molecular mechanism of H.pylori infection-associated gastric intestinal metaplasia, and provides the mechanism of a novel H. pylori virulence factor SlyD in gastric precancerous disease.
2024-11-26 | GSE282336 | GEO
Project description:Caspases regulate cell death programs in response to environmental stresses, including infection and inflammation, and are therefore critical for the proper operation of the mammalian immune system. Caspase-8 is necessary for optimal production of inflammatory cytokines and host defense against infection by multiple pathogens including Yersinia, but whether this is due to death of infected cells or an intrinsic role of caspase-8 in TLR-induced gene expression is unknown. Caspase-8 activation at death signaling complexes results in its autoprocessing and subsequent cleavage and activation of its downstream apoptotic targets. Whether caspase-8 activity is also important for inflammatory gene expression during bacterial infection has not been investigated. Here, we report that caspase-8 plays an essential cell-intrinsic role in innate inflammatory cytokine production in vivo during Yersinia infection. Unexpectedly, we found that caspase-8 enzymatic activity regulates gene expression in response to bacterial infection as well as TLR signaling independently of apoptosis. Using newly-generated mice in which caspase-8 autoprocessing is ablated (Casp8DA/DA), we now demonstrate that caspase-8 enzymatic activity, but not autoprocessing, mediates induction of inflammatory cytokines by bacterial infection and a wide variety of TLR stimuli. Because unprocessed caspase-8 functions in an enzymatic complex with its homolog cFLIP, our findings implicate the caspase-8/cFLIP heterodimer in control of inflammatory cytokines during microbial infection, and provide new insight into regulation of antibacterial immune defense.
2016-09-15 | GSE86922 | GEO
Project description:Tuberculosis results from an interaction between a chronically persistent pathogen counteracted by IFN-g-mediated immune responses. Modulation of IFN-g signaling could therefore constitute a major immune evasion mechanism for M. tuberculosis. SOCS1 plays a major role in the inhibition of IFN-g-mediated responses. We found that M. tuberculosis infection stimulates SOCS1 expression in mouse and human myeloid cells. Significantly higher levels of SOCS1 were induced after in vitro or in vivo infection with virulent M. tuberculosis-than with attenuated M. bovis BCG. Different innate and adaptive immune mechanisms participated in infection-induced SOCS1 expression. SOCS1 hampered M. tuberculosis clearance both in macrophages and during murine infection in vivo. On the other hand, SOCS1 protected the host from an infection-induced inflammation. Despite SOCS1 expression, mycobacteria-infected macrophages were not tolerant to IFN-g. Instead, an impaired IFN-g secretion by macrophages, associated to lower responses to IL-12, accounted for the increased mycobacterial intracellular growth in presence of SOCS1. SOCS1 attenuated the expression of the majority of genes modulated by infection of macrophages (6,1% of the transcriptome), indicating the relevance of the molecule in the outcome of infection with M. tuberculosis. We suggest that SOCS1 is expressed during M. tuberculosis infection to establish a successful chronic infection, and dampen inflammatory damage. Difference in genotype and TB infection comparison
2012-01-18 | GSE23508 | GEO