Chicken gut metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA277051 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2052450.fastq.gz | Fastqsanger.gz | |||
| SRR2052460.fastq.gz | Fastqsanger.gz | |||
| SRR2052470.fastq.gz | Fastqsanger.gz | |||
| SRR2052451.fastq.gz | Fastqsanger.gz | |||
| SRR2052461.fastq.gz | Fastqsanger.gz |
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Project description:Campylobacter jejuni is the major cause of acute gastroenteritis in the developed world. It is usually acquired through contaminated poultry as C. jejuni causes a silent asymptomatic infection of the chicken. Pathogens face different sources of stress during its transit through the gut. In this study, we describe the ability of C. jejuni to survive nitrosative stress at very low oxygen levels that reflect those in hypoxic gut environments. Specifically, we here explore an innovative model of signal recognition during colonization. We use a diffusion capsule to feed small, diffusible molecules from chicken caecal matter into a microaerobic C. jejuni culture to study the transcriptomic changes mounted as response to chemical signals present in the chicken gut. We find that in early stages of exposure to the caecal contents (10 min) the dual component colonization regulator, dccR, plays an important yet not fully understood role. Although the caecal material contains cyanide derived from plant sources, we find no role for a truncated globin (encoded by ctb), which has previously been implicated in resistance to this haem ligand.
2012-08-07 | GSE39917 | GEO
Project description:Campylobacter jejuni is a common cause of diarrheal disease worldwide. Human infection typically occurs through the ingestion of contaminated poultry products. We previously demonstrated that an attenuated Escherichia coli live vaccine strain expressing the C. jejuni N-glycan on its surface reduces the Campylobacter load in more than 50% of vaccinated leghorn and broiler birds to undetectable levels (responder birds), whereas the remainder of the animals were still colonized (non-responders). To understand the underlying mechanism, we conducted 3 larger scale vaccination and challenge studies using 135 broiler birds and found a similar responder/non responder effect. The submitted data were used for a genome-wide association study of the chicken responses to glycoconjugate vaccination against Campylobacter jejuni.
2021-11-01 | GSE181619 | GEO
Project description:The gut of chicken is mostly colonised with Campylobacter jejuni and with 100 fold less C. coli. The competitive ability of C. coli OR12 over C. jejuni OR1 has been examined in experimental broiler chickens following the observation that C. coli replaced an established C. jejuni intestinal colonisation within commercial chicken flocks reared outdoors (El-Shibiny, A., Connerton, P.L., Connerton, I.F., 2005. Enumeration and diversity of campylobacters and bacteriophages isolated during the rearing cycles of free-range and organic chickens. Applied Environmental Microbiology. 71, 1259-1266).
2015-09-15 | GSE17805 | GEO
Project description:RNAseq analysis of caecal tissue from 14 C. jejuni-susceptible and 14 C. jejuni-resistant birds from a single population of infected chickens was conducted in order to identify gene expression associated with resistance to colonization. Significantly higher expression of genes involved in the innate immune response, cytokine signaling, B cell and T cell activation and immunoglobulin production, as well as the renin-angiotensin system was observed in resistant birds. A population of 255 Barred Rock chickens were orally inoculated with C. jejuni and their caecal colonization levels estimated 48 hours post-inoculation. Caecal samples from 14 birds with no colonization and the 14 birds with the highest colonization were selected for mRNA sequencing.
2013-02-15 | E-GEOD-44341 | biostudies-arrayexpress
Project description:Campylobacter-infected chicken caecal tonsils
| PRJEB22580 | ENA
Project description:Campylobacter jejuni (C. jejuni) is a zoonotic pathogen that causes human diarrhea worldwide. Chickens are a natural reservoir of C. jejuni. Understanding the host response to C. jejuni infection at the molecular level will lay the foundation to control human campylobacterosis by reducing food contamination. Two distinct genetic lines, resistant (line A) and susceptible (line B) to C. jejuni colonization, were utilized to profile the host response to C. jejuni infection using an Agilent chicken 44K microarray. Day-old chickens were challenged orally with C. jejuni and spleens collected for total RNA 7 days post-challenge. Twenty infected samples with highest (a) or lowest bacterial number (b) in cecal content and twenty non-infected (c) in each line were randomly pooled into four biological replicates. The pair comparisons among these three groups within each line were analyzed. The signal intensity of each gene was normalized using LOWESS method. A mixed model was used to identify differentially expressed genes by SAS (P < 0.001). This was opposite to previous cecal tonsil microarray result. There were 468, 743, and 939 genes differentially expressed between groups a and c, groups a and b, and groups b and c in line A, respectively, and 201, 37, 126 genes in line B, respectively. More differentially expressed genes in spleen in line A than in line B were found. The results indicated that significantly different response to C. jejuni infection occurred between resistant and susceptible chicken lines, and the effects of interaction between genetics and tissue should be considered.
2011-01-01 | GSE18541 | GEO
Project description:Campylobacter jejuni strain:chicken | isolate:chicken Genome sequencing
| PRJNA492384 | ENA
Project description:It is essential to understand host response to Campylobacter jejuni infection in order to genetically improve resistance to its colonization in chickens. A custom Agilent chicken 44K array was used to examine gene expression profiles after Campylobacter jejuni infection of two broiler lines (A and B). Day-old chicks were orally inoculated with C. jejuni. After day 7 post-infection, the cecal tonsil was collected for total RNA isolation and cecal content for bacteria burden quantification. Twenty highest and lowest bacterial burden birds and non-infected birds within each line were used to pool four biological replicates for each group. The pair comparisons among high, low bacterial burden, and non-infected group were used. The signal intensity of each gene was normalized by LOWESS method. A mixed model including the fixed effects of dye, line, treatment and line × treatment interaction, and random effects of slide and array was used to identify differentially expressed genes at P < 0.001 by SAS program. Within line A, there were 61, 163, and 90 genes significantly differentially expressed between high and low bacterial burden, high bacterial burden and non-infected group, and low bacterial burden and non-infected group, respectively; 2637, 1684, 561 genes within line B, respectively. The results suggested that genetics, treatment and genetics × treatment interaction played important role in gene regulation of C. jejuni infection. The findings in the current study will lead the identification of potential candidate genes for genetic resistance to C. jejuni infection in chickens. Keywords: diease state analysis
2010-08-03 | GSE10257 | GEO
Project description:The gut of chicken is mostly colonised with Campylobacter jejuni and with 100 fold less C. coli. The competitive ability of C. coli OR12 over C. jejuni OR1 has been examined in experimental broiler chickens following the observation that C. coli replaced an established C. jejuni intestinal colonisation within commercial chicken flocks reared outdoors (El-Shibiny, A., Connerton, P.L., Connerton, I.F., 2005. Enumeration and diversity of campylobacters and bacteriophages isolated during the rearing cycles of free-range and organic chickens. Applied Environmental Microbiology. 71, 1259-1266). Five independent DNA preps of C. jejuni RM1221 were labelled with Cy 5 independently and they were mixed well which was used as the control. OR1 and OR12 were labelled with Cy 3 independently and equal concentration of the control and sample DNA were used for hybridisation. Three biological replicates were done for each slide. The supplementary file (linked at the foot of this record) represents the averaged normalised values for each experimental condition (3replicates/experimental condition).
2015-09-15 | E-GEOD-17805 | biostudies-arrayexpress
Project description:Chromosomal structural variation can cause alterations in gene dosage and gene regulation between genomes. Structural variants producing a change in the number of copies of a genomic region are termed copy number variants (CNVs). CNVs have been demonstrated to have causative effects on both Mendelian and complex traits, including susceptibility to infectious diseases. We are interested in mapping CNVs to domesticated chicken breeds to help determine structural variation between genomes that influences economically important traits. For this study, Fayoumi, Leghorn, Line A broiler and Line B broiler chicken were chosen. Fayoumi and Leghorn chickens were selected as these two breeds harbor different responses certain pathogens like Avian Influenza Virus and coccidiosis; Broiler Line A and Line B indivduals were chosen as they harbor different intestinal colonization loads to the bacterium Campylobacter jejuni. Campylobacter genetic Line A and genetic Line B are from a commercial producer have been previously described as either resistant (Line A) or susceptible (Line B). Highly inbred chicken lines Fayoumi M15.2 (n=6) and Leghorn GHs6 (n=6) and broilers from Line A (n=24 individuals in pools of 4) and Line B (n=24 individuals in pools of 4)were subjected to array Comparative Genomic Hybridization (aCGH). Each sample was normalized to a Red Jungle Fowl reference. CNVs for each individual and between lines were determined. The major goal of this study was to discover and characterize CNVs in chickens to further narrow in on Quantitative Trait Loci (QTLs) affecting disease response.
2016-02-11 | GSE44440 | GEO