Mouse gut metagenome
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ABSTRACT:
PROVIDER: PRJNA211485 | ENA |
REPOSITORIES: ENA
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Project description:Consumption of contaminated poultry products is one of the main sources of human campylobacteriosis, of which Campylobacter jejuni subsp. jejuni (C. jejuni) and C. coli are responsible for approximately 98% of the cases. The ceca of commercial turkeys are the main anatomical site where Campylobacter asymptomatically colonizes. We have previously colonized the ceca of commercial turkey poults with C. jejuni, and demonstrated acute changes in cytokine gene expression in cecal tissue and histologically scored intestinal lesions at 2 days post-inoculation (dpi). The host-response of turkeys to C. coli colonization is unknown. Cecal tonsils (CT) are an important part of the gastrointestinal-associated lymphoid tissue that function to sample material passing in and out of the ceca and generating immune responses against intestinal pathogens. The CT immune response towards Campylobacter is unknown. In this study, we generated a C. coli kanamycin-resistant construct (CcK) for enumeration from cecal contents after experimental challenge. In vitro analysis of CcK demonstrated no changes in motility when compared to the parent isolate, but in vitro growth rates were significantly different than the parent strain. Poults were inoculated by oral gavage with CcK (5x10^7 cfu) or sterile-media (mock-colonized), and euthanized at 1 and 3 dpi. At both time points, CcK was recovered from cecal contents, but not from the mock-colonized group. As a marker of acute inflammation, serum alpha-1 acid glycoprotein was significantly elevated at 3 dpi in CcK inoculated poults compared to mock-infected samples. Significant histological lesions were detected in cecal and CT tissues of CcK colonized poults at 1 and 3 dpi, respectively. RNAseq analysis identified 250 differentially expressed genes (DEG) in CT from CcK colonized poults at 3 dpi, of which 194 were upregulated and 56 were downregulated. From the DEG, 9 significantly enriched biological pathways were identified, including platelet aggregation, response to oxidative stress and negative regulation of oxidative stress-induced intrinsic apoptotic signaling pathway. These data suggest that C. coli induced an acute inflammatory response in the intestinal tract of poults, and that platelet aggregation and oxidative stress in the CT may affect the turkey’s ability to resist Campylobacter colonization. Results from this study provide insight into host-response of the turkey CT to Campylobacter colonization. These findings will help to develop and test Campylobacter mitigation strategies to promote food safety in commercial turkeys.
2020-10-01 | GSE158639 | GEO
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: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. Chickens in two broiler lines were inoculated with 10^5 cfu C. jejuni on one day after hatch. The cecal content and cecal tonsil was collected and bacterial number in cecal content was counted on day 7 after inoculation. Twenty samples were separated into 3 groups (high burden, low burden, and control) based on bacterial burden of cecal content in each line, 5 samples were mixed randomly into one pool. A dual color, balanced design was carried on for all samples. Three comparisons were used in each line, non-infected/susceptible, susceptible/resistant, resistant/non-infected, totally, four biological replicates in each line. A Dye swap was used in each pair of comparisons including AN/AS, AS/AR, AR/AN; BN/BS, BS/BR, and BR/BN. Background subtracted signal intensity were collected from 24 arrays and normalized for data analysis.
2011-01-01 | E-GEOD-18541 | biostudies-arrayexpress
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 is the prevalent cause of bacterial gastroenteritis in human worldwide. The ability to survive stomach acidity is a fundamental requirement for C. jejuni to colonize the host and cause disease. However, the mechanism of C. jejuni acid survival is still unknown. Herein, we demonstrated that C. jejuni is able to survive acidic conditions at pH 4 up to 8 min without a drop in viability. The acid stimulon of C. jejuni 81-176 revealed the up-regulation of many genes important for Campylobacter acid survival such as heat shock genes and genes involved in energy metabolism. On the other hand, the repression of ribosomal genes highlights the ability of C. jejuni to direct its machinery to survive stressful conditions. Prior acid exposure cross-protected C. jejuni against oxidative stress suggesting an overlap in C. jejuni’s responses to various stresses. Interestingly, the induced expression of virulence genes in C. jejuni upon acid exposure such as the Campylobacter invasion antigen (ciaB) indicates that acid stress plays a role in C. jejuni host pathogenesis. Acid exposure significantly enhanced C. jejuni pathogenesis in both eukaryotic cells and G. melonella. To the best of our knowledge, this is the first study characterizes the influence of acid stress on C. jejuni pathogenesis in an infection model. Altogether, this study uncovers the transcriptional profile of C. jejuni in response to acidic conditions as those encountered in the stomach. In addition, our results demonstrate that acid stress jump-starts C. jejuni for efficient gut colonization and host pathogenesis. Campylobacter jejuni is the prevalent cause of bacterial gastroenteritis in human worldwide. The ability to survive stomach acidity is a fundamental requirement for C. jejuni to colonize the host and cause disease. However, the mechanism of C. jejuni acid survival is still unknown. Herein, we demonstrated that C. jejuni is able to survive acidic conditions at pH 4 up to 8 min without a drop in viability. The acid stimulon of C. jejuni 81-176 revealed the up-regulation of many genes important for Campylobacter acid survival such as heat shock genes and genes involved in energy metabolism. On the other hand, the repression of ribosomal genes highlights the ability of C. jejuni to direct its machinery to survive stressful conditions. Prior acid exposure cross-protected C. jejuni against oxidative stress suggesting an overlap in C. jejuni’s responses to various stresses. Interestingly, the induced expression of virulence genes in C. jejuni upon acid exposure such as the Campylobacter invasion antigen (ciaB) indicates that acid stress plays a role in C. jejuni host pathogenesis. Acid exposure significantly enhanced C. jejuni pathogenesis in both eukaryotic cells and G. melonella. To the best of our knowledge, this is the first study characterizes the influence of acid stress on C. jejuni pathogenesis in an infection model. Altogether, this study uncovers the transcriptional profile of C. jejuni in response to acidic conditions as those encountered in the stomach. In addition, our results demonstrate that acid stress jump-starts C. jejuni for efficient gut colonization and host pathogenesis.
2016-10-01 | GSE73793 | GEO
Project description:Comparison of the Campylobacter jejuni NCTC 11168 proteome in MH media in the presence and absence of Deoxycholate
2017-11-21 | PXD005306 | Pride
Project description:Cj0440c encodes a putative transcriptional regulator. To determine the role of Cj0440c in C.jejuni, we knocked out Cj0440c in the wild-type strain (S) to obtain the Cj0440c mutants (SM). Then we compared the transcriptome of the Cj0440c mutant with that of the parent strain using DNA microarray. These comparisons identified 19 genes that showed aM-bM-^IM-%2-fold change in expression in SM. The differentially expressed genes in SM encode proteins involved in flagellar biosynthesis, O-linked glycosylation and hypothetical proteins with unknown fuctions. Cj0440c may regulate flagellar structural element expression or as a compenent of flagellar complex co-expressed with other flagellar genes. Subsequent experiments demonstrated that inactivation of Cj0440c affected corresponding phenotypes of C.jejuni, including broken flagella, weaker motility and reduced colonization ability in chickens. These findings indicate that Cj0440c governs the expression of multiple genes related to flagellar biosynthesis and O-linked glycosylation. This study provides favorable evidence for completing the information of the Campylobacter jejuni genome. An eight chip study using total RNA recoverd from four separate wild-type cultures of Campylobacter jejuni NCTC111168 (S) and four separate cultures of a mutant strain, Campylobacter jejuni NCTC11168 delta- Cj0440c (SM), in which Cj0440c is deleted. Each chip measures the expression level of 1634 genes from Campylobacter jejuni NCTC11168.
2013-08-13 | E-GEOD-49256 | biostudies-arrayexpress
Project description:Cj0440c, a putative transcriptional regulator, was over-expressed in the high-level erythromycin-resistant (Eryr) Campylobacter jejuni strains. To determine the role of Cj0440c on the development and fitness of erythromycin resistance in C. jejuni, we knocked out Cj0440c in Eryr strain (R) to obtain the Cj0440c mutants (RM). Then we compared the transcriptome of the Cj0440c mutant with that of the parent strain using DNA microarray. These comparisons identified 9 genes that showed a M-bM-^IM-%2-fold change in expression in RM. The differentially expressed genes in RM are related to flagellar biosynthesis and unknown functions. What's more, katA, encoding catalase, down-regulated in RM. Cj0440c may progress flagellar genes expression, help to escape drug pressure and disseminate and colonize smoothly, and Cj0440c in Eryr Campylobacter may protect bacteria from harmful oxygen stress from the host immune system, other microorganism in host intestinal and its own products. These findings indicate that Cj0440c is essential for the fitness (growth) of resistant C. jejuni by controlling the expression of several genes involved in flagellar assembly and catalase, enhancing cell motility for colonization and invasion under the pressure of drug. This study widened our understanding on the molecular mechanism of resistance and provides scientific reference for drug research and application. An eight-chip study using total RNA recoverd from four separate resistant-type cultures of Erythrocin-resistant Campylobacter jejuni NCTC 111168 (R) and four separate cultures of a mutant strain, erythrocin-resistant Campylobacter jejuni NCTC 11168 delta- Cj0440c (RM), in which Cj0440c is deleted. Each chip measures the expression level of 1634 genes from Campylobacter jejuni NCTC 11168.
2013-08-13 | E-GEOD-49255 | biostudies-arrayexpress
Project description:Campylobacter spp. cause food-borne illnesses worldwide due to contaminated food and cross-contamination. This is at least partly the result of Campylobacter resistance in the food production chain, as modern food production facilitates the emergence and spread of resistance through intensive use of antimicrobials and international trade in raw materials and food products. The biofilm 'lifestyle' of Campylobacter contributes to this spread as it enables them to withstand stress in the environment both outside and inside the host. Campylobacter adhesion and biofilm formation has major implications for the food industry, where biofilms can be persistent sources of contamination. In our study, we described how the proteome of C. jejuni is affected by the deletion of the luxS gene on the planktonic cell type of C. jejuni, which is the first step of biofilm formation. In C. jejuni, the presence of the luxS gene has been associated with several phenotypes, including intercellular signalling, motility, biofilm formation, host colonisation, virulence, autoagglutination, cellular adherence and invasion, oxidative stress and chemotaxis. Deletion of the luxS gene is associated with a reduction or absence of the above properties compared to wild type (Elvers and Park, 2002; Guerry et al., 2006; He et al., 2008; Jeon et al., 2003; Quiñones et al., 2009; Plummer et al., 2011; Plummer, 2012; Reeser et al., 2007).
2023-01-24 | PXD035008 | Pride
Project description:Although the major food-borne pathogen Campylobacter jejuni has been isolated from diverse animal, human and environmental sources, our knowledge of genomic diversity in C. jejuni is based exclusively on human or human food-chain-associated isolates. Studies employing multilocus sequence typing have indicated that some clonal complexes are more commonly associated with particular sources. Using comparative genomic hybridization on a collection of 80 isolates representing diverse sources and clonal complexes, we identified a separate clade comprising a group of water/wildlife isolates of C. jejuni with multilocus sequence types uncharacteristic of human food-chain-associated isolates. By genome sequencing one representative of this diverse group (C. jejuni 1336), and a representative of the bank-vole niche specialist ST-3704 (C. jejuni 414), we identified deletions of genomic regions normally carried by human food-chain-associated C. jejuni. Several of the deleted regions included genes implicated in chicken colonization or in virulence. Novel genomic insertions contributing to the accessory genomes of strains 1336 and 414 were identified. Comparative analysis using PCR assays indicated that novel regions were common but not ubiquitous among the water/wildlife group of isolates, indicating further genomic diversity among this group, whereas all ST-3704 isolates carried the same novel accessory regions. While strain 1336 was able to colonize chicks, strain 414 was not, suggesting that regions specifically absent from the genome of strain 414 may play an important role in this common route of Campylobacter infection of humans. We suggest that the genomic divergence observed constitutes evidence of adaptation leading to niche specialization. Data is also available from <ahref=http://bugs.sgul.ac.uk/E-BUGS-95 target=_blank>BuG@Sbase</a>
2011-04-15 | E-BUGS-95 | biostudies-arrayexpress