Mouse gut metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA348350 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR21704967_1.fastq.gz | Fastqsanger.gz | |||
| SRR21704967_2.fastq.gz | Fastqsanger.gz | |||
| SRR21704968_1.fastq.gz | Fastqsanger.gz | |||
| SRR21704968_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 1954 |
Similar Datasets
Project description:Humans and animals encounter a summation of exposures during their lifetime (the exposome). In recent years, the scope of the exposome has begun to include microplastics. Microplastics (MPs) have increasingly been found in locations where there could be an interaction with Salmonella enterica Typhimurium, one of the commonly isolated serovars from processed chicken. In this study, the microbiota response to a 24-hour co-exposure to Salmonella enterica Typhimurium and/or low-density polyethylene (PE) microplastics in an in vitro broiler cecal model was determined using 16S rRNA amplicon sequencing (Illumina) and untargeted metabolomics. Community sequencing results indicated that PE fiber with and without S. Typhimurium yielded a lower Firmicutes/Bacteroides ratio compared to other treatment groups, which is associated with poor gut health, and overall had greater changes to the cecal microbial community composition. However, changes in the total metabolome were primarily driven by the presence of S. Typhimurium. Additionally, the co-exposure to PE Fiber and S. Typhimurium caused greater cecal microbial community and metabolome changes than either exposure alone. Our results indicate that polymer shape is an important factor in effects resulting from exposure. It also demonstrates that microplastic-pathogen interactions cause metabolic alterations to the chicken cecal microbiome in an in vitro chicken cecal model.
2024-07-08 | MTBLS9001 | MetaboLights
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:Bacterial genotoxins, produced by several Gram-negative bacteria, induce DNA damage in the target cells. While the responses induced in the host cells have been extensively studied in vitro, the role of the genotoxins as effectors during the course of acute and chronic infections remains poorly characterized.To address this issue, we assessed the effects of the Salmonella enterica genotoxin, known as typhoid toxin, in in vivo models of murine chronic infections. Immunocompetent mice were chronically infected with isogenic S. enterica, serovar Typhimurium (S. Typhimurium) strains, encoding either a functional (MC71-TT) or an inactive (MC71-DcdtB) typhoid toxin. Keywords: salmonella typhimurium, bacterial genotoxins, typhoid toxin, chronic infection, mice model
2016-03-31 | GSE72046 | GEO
Project description:Longitudinal analysis of Salmonella typhimurium mRNA from superspeader mouse cecal content and stool compared to in vitro Salmonella typhimurium mRNA.
2023-03-22 | GSE207764 | GEO
Project description:To investigate the extent to which macrophages respond to Salmonella infection, researchers infected RAW 264.7 macrophages with Salmonella enterica serotype Typhimurium and analyzed macrophage proteins at various time points following infection by using a global proteomic approach.
2013-10-07 | PXD000389 | Pride
Project description:The deposited microarray data were generated in a study that integrated the gene expression profiles and metabolic responses of Caco2 cells incubated with Bifidobacterium infantis subsp. infantis and Salmonella enterica subsp. enterica sv. Typhimurium. The aim of this study was to investigate the interaction of B. infantis, S. Typhimurium, and host cells (Caco2) in the course of infection to understand the molecular mechanics of probiotic-pathogen-host interactions.
2024-05-08 | GSE266880 | GEO
Project description:Salmonella enterica serotype Typhimurium causes an acute inflammatory reaction in the cecum of streptomycin pre-treated mice. We determined global changes in gene expression elicited by serotype Typhimurium in the cecal mucosa. The gene expression profile was dominated by T cell derived cytokines and genes whose expression is known to be induced by these cytokines. Markedly increased mRNA levels of interferon (IFN) ï§, interleukin (IL) 22 and IL-17 were detected by quantitative real-time PCR. Furthermore, mRNA levels of genes whose expression is induced by IFNï§, IL-22 or IL-17, including macrophage inflammatory protein (MIP)-2, inducible nitric oxide synthase (iNOS), lipocalin-2, MIP-1ï¡, MIP-1ï¢, and keratinocyte-derived cytokine (KC), were also markedly increased. To assess the importance of T cells in orchestrating this pro-inflammatory gene expression profile, we depleted T cells using a monoclonal antibody prior to investigating cecal inflammation caused by serotype Typhimurium in streptomycin pre-treated mice. Depletion of CD3+ T cells resulted in a dramatic reduction in gross pathology, a significantly reduced recruitment of neutrophils and a marked reduction in mRNA levels of IFNï§, IL-22, IL-17, iNOS, lipocalin-2 and KC. Our results suggest that T cells play an important role in amplifying inflammatory responses induced by serotype Typhimurium in the cecal mucosa. Experiment Overall Design: Determine global changes in gene expression elicited by serotype Typhimurium in the cecal mucosa. For each condition, control and infected, total cecal RNA from 4 mice was pooled
2008-04-07 | E-GEOD-10594 | biostudies-arrayexpress
Project description:Infection with Salmonella enterica serovar Typhi in humans causes the systemic, life-threatening disease typhoid fever. In the laboratory, typhoid fever can be modeled through the inoculation of susceptible mice with Salmonella enterica serovar Typhimurium. The ensuing disease is characterized by systemic dissemination and colonization of many organs, including the liver, spleen and gallbladder. Using this murine model, we previously characterized the interactions between Salmonella Typhimurium and host cells in the gallbladder and showed that this pathogen can successfully invade gallbladder epithelial cells and proliferate. Additionally, we showed that Salmonella Typhimurium can use bile phospholipids to grow at high rates. These abilities are likely important for quick colonization of the gallbladder during typhoid fever and further pathogen dissemination through fecal shedding. To further characterize the interactions between Salmonella and the gallbladder environment we compared the transcriptome of Salmonella cultures grown in LB or physiological murine bile. Our data showed that many genes involved in bacterial central metabolism are affected by bile, with the citric acid cycle being repressed and alternative respiratory systems being activated. Additionally, our study revealed a new aspect of Salmonella interactions with bile through the identification of phoP as a bile-responsive gene. Repression of phoP expression does not involve PhoPQ sensing of a bile component. Due to its critical role in Salmonella virulence, further studies in this area will likely reveal aspects of the interaction between Salmonella and bile that are relevant to disease.
2011-11-10 | GSE33604 | GEO
Project description:Bacterial genotoxins, produced by several Gram-negative bacteria, induce DNA damage in the target cells. While the responses induced in the host cells have been extensively studied in vitro, the role of the genotoxins as effectors during the course of acute and chronic infections remains poorly characterized.To address this issue, we assessed the effects of the Salmonella enterica genotoxin, known as typhoid toxin, in in vivo models of murine chronic infections. Immunocompetent mice were chronically infected with isogenic S. enterica, serovar Typhimurium (S. Typhimurium) strains, encoding either a functional (MC71-TT) or an inactive (MC71-DcdtB) typhoid toxin. Keywords: salmonella typhimurium, bacterial genotoxins, typhoid toxin, chronic infection, mice model Transcriptomic analysis was performed on intestine tissues (colon, jejunum and ileum) and liver collected from 129S6/SvEvTac mice, either uninfected or infected with S. typhimurium MC71 strains (strain MC71-TT, expressing a functional typhoid toxin, and strain MC71-dcdtB, expressing an inactive typhoid toxin) for 60 days
2016-03-31 | E-GEOD-72046 | biostudies-arrayexpress
Project description:It is becoming increasingly clear that cells infected with pathogens can signal to bystander cells. Infected cells have the ability to alert and instruct bystander cells to mount pro-inflammatory cytokine response, thus contributing to clearing infections. Here we analyse secretome of HeLa cells infected with Salmonella enterica serovar Typhimurium strain SL1344. Cells were infected with a MOI of 100 for 14 hours. Secretome from mock- and Salmonella-infected cells was collected for mass-spectrometry analysis.
2021-04-16 | PXD018026 | Pride