Evolution of Campylobacter in a long-term human host
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ABSTRACT:
PROVIDER: PRJEB18520 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1750950_1.fastq.gz | Fastqsanger.gz | |||
| ERR1750950_2.fastq.gz | Fastqsanger.gz | |||
| ERR1750960_1.fastq.gz | Fastqsanger.gz | |||
| ERR1750960_2.fastq.gz | Fastqsanger.gz | |||
| ERR1750951_1.fastq.gz | Fastqsanger.gz |
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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:Campylobacter jejuni is a widespread pathogen responsible for most of the food-borne gastrointestinal diseases in Europe. For pathogen control in the food industry, the use of natural antimicrobial molecules is a promising strategy to avoid antibiotic treatments. Isothiocyanates are natural antimicrobial compounds which also display anti-cancer activity. Several studies described the chemoprotective effect of isothiocyanates on eukaryotic cells, but the antimicrobial mechanism is still poorly understood. We investigated the early cellular response of C. jejuni to benzylisothiocyanate (BITC) by both transcriptomic and physiological (respirometry, ATP content measurements and isolations of aggregated proteins).
2013-09-19 | GSE45823 | GEO
Project description:Objectives: The aim of the study was to investigate the Campylobacter jejuni response to subinhibitory concentrations of natural antimicrobial compound pinocembrin
2017-08-31 | GSE72760 | 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:Growth of Campylobacter jejuni in butyrate, including deletions of a TCS involved in sensing this response
2021-01-01 | GSE142852 | GEO
Project description:Background: During gut colonization, the enteric pathogen C. jejuni has to surmount the toxic effects of reactive oxygen species produced by its own metabolism, by the host immune system and by the intestinal microflora. Elucidation of C. jejuni oxidative stress defense mechanisms is critical for understanding Campylobacter pathophysiology. Results: The mechanisms of oxidative stress defenses in Campylobacter jejuni were characterized by transcriptional profiling, genes mutagenesis, and phenotypic analysis. The transcriptome changes, in response to H2O2, cumene hydroperoxide, or menadione exposure, were found to be oxidant specific and revealed the differential expression of genes belonging to a variety of biological pathways, from the classical oxidative stress defense systems, to the heat shock response, DNA repair and metabolism, fatty acid and capsule biosynthesis, and multidrug efflux pumps. To define the peroxide sensing regulator PerR, an isogenic mutant was constructed and its transcriptome profile compared to the wild-type strain. Sixty-six genes were found to belong to the PerR regulon. PerR appear to regulate gene expression both dependently and independently of the presence of iron and/or H2O2. The perR mutant was affected in its motility and attenuated in the chick colonization model. Mutagenic and phenotypic studies of the superoxide disumutase SodB, the alkyl-hydroxyperoxidase AhpC, and the catalase KatA, revealed their role in oxidative stress defenses and chick gut colonization. Conclusion: This study reveals the interplay between PerR, the iron metabolism and the oxidative stress defenses and highlights their role in the colonization and/or survival of C. jejuni in the chick cecum. Keywords: Transcriptional response to 3 oxidants (H2O2, menadione and cumene hydroperoxide) and characterization of the perR regulon (comparison of the transciptomes from the wild-type and perR mutant).
2010-09-07 | GSE13126 | GEO
Project description:Background: The food-borne pathogen Campylobacter is one of the most important zoonotic pathogens. Compared to other zoonotic bacteria, Campylobacter species are quite susceptible to environmental or technological stressors. This might be due to the lack of many stress response mechanisms described in other bacteria. Nevertheless, Campylobacter is able to survive in the environment and food products. Although some aspects of the heat stress response in Campylobacter (C.) jejuni are already known, information about the heat stress response in the related species C. coli and C. lari are still unknown. Results: The stress response to elevated temperatures (46°C) was investigated by survival assays and whole transcriptome analyses for the strain C. jejuni NCTC11168, C. coli RM2228 and C. lari RM2100. While C. jejuni showed highest thermotolerance followed by C. lari and C. coli, none of the strains survived at this temperature for more than 24 hours. Transcriptomic analyses revealed that only 3 % of the genes in C. jejuni and approx. 20 % of the genes of C. coli and C. lari were differentially expressed after heat stress, respectively. The transcriptomic profiles showed enhanced gene expression of several chaperones like dnaK, groES, groEL and clpB in all strains, but differences in the gene expression of transcriptional regulators like hspR, perR as well as for genes involved in metabolic pathways, translation processes and membrane components. However, the function of many of the differentially expressed gene is unknown so far. Conclusion: We could demonstrate differences in the ability to survive at elevated temperatures for C. jejuni, C. coli and C. lari and showed for the first time transcriptomic analyses of the heat stress response of C. coli and C. lari. Our data suggest that the heat stress response of C. coli and C. lari are more similar to each other compared to C. jejuni, even though on genetic level a higher homology exists between C. jejuni and C. coli. This indicates that stress response mechanisms described for C. jejuni might be unique for this species and not necessarily transferable to other Campylobacter species.
2020-03-04 | GSE67468 | GEO
Project description:Background: The food-borne pathogen Campylobacter is one of the most important zoonotic pathogens. Compared to other zoonotic bacteria, Campylobacter species are quite susceptible to environmental or technological stressors. This might be due to the lack of many stress response mechanisms described in other bacteria. Nevertheless, Campylobacter is able to survive in the environment and food products. Although some aspects of the heat stress response in Campylobacter (C.) jejuni are already known, information about the heat stress response in the related species C. coli and C. lari are still unknown. Results: The stress response to elevated temperatures (46°C) was investigated by survival assays and whole transcriptome analyses for the strain C. jejuni NCTC11168, C. coli RM2228 and C. lari RM2100. While C. jejuni showed highest thermotolerance followed by C. lari and C. coli, none of the strains survived at this temperature for more than 24 hours. Transcriptomic analyses revealed that only 3 % of the genes in C. jejuni and approx. 20 % of the genes of C. coli and C. lari were differentially expressed after heat stress, respectively. The transcriptomic profiles showed enhanced gene expression of several chaperones like dnaK, groES, groEL and clpB in all strains, but differences in the gene expression of transcriptional regulators like hspR, perR as well as for genes involved in metabolic pathways, translation processes and membrane components. However, the function of many of the differentially expressed gene is unknown so far. Conclusion: We could demonstrate differences in the ability to survive at elevated temperatures for C. jejuni, C. coli and C. lari and showed for the first time transcriptomic analyses of the heat stress response of C. coli and C. lari. Our data suggest that the heat stress response of C. coli and C. lari are more similar to each other compared to C. jejuni, even though on genetic level a higher homology exists between C. jejuni and C. coli. This indicates that stress response mechanisms described for C. jejuni might be unique for this species and not necessarily transferable to other Campylobacter species.
2020-03-04 | GSE67466 | GEO
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:Campylobacter jejuni is the most prevalent cause of foodborne bacterial enteritis worldwide. This study aims at the characterisation of pathomechanisms and signalling in Campylobacter-induced diarrhoea in the human mucosa. During routine colonoscopy, biopsies were taken from patients suffering from campylobacteriosis. RNA-seq of colon biopsies was performed to describe Campylobacter jejuni-mediated effects. Mucosal mRNA profiles of acutely infected patients and healthy controls were generated by deep sequencing using Illumina HiSeq 2500. This data provide the basis for subsequent upstream regulator analysis.
2017-10-10 | GSE88710 | GEO