Campylobacter jejuni
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PROVIDER: PRJNA92879 | ENA |
REPOSITORIES: ENA
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Project description:Campylobacter jejuni is a highly prevalent food-borne pathogen that causes diarrhoeal disease in humans. A natural zoonotic, it must overcome significant stresses both in vivo and during transmission despite the absence of several traditional stress response genes. Its ability to interact with and invade human intestinal epithelial cells closely correlates with virulence. A C. jejuni microarray-based screen revealed that several known virulence genes and several uncharacterized genes, including spoT, were rapidly upregulated during infection of human epithelial cells. spoT and its homologue relA have been shown in other bacteria to regulate the stringent response, an important stress response that to date had not been demonstrated for C. jejuni. We have found that C. jejuni mounts a stringent response that is regulated by spoT. Detailed analyses of a C. jejuni delta spoT mutant revealed that the stringent response is required for several specific stress, transmission and antibiotic resistance-related phenotypes. These include stationary phase survival, growth and survival under low CO2/high O2 conditions, and rifampicin resistance. A secondary suppressor strain that specifically rescues the low CO2 growth defect of the delta spoT mutant was also isolated. The stringent response additionally proved to be required for the virulence-related phenotypes of adherence, invasion, and intracellular survival in two human epithelial cell culture models of infection; spoT is the first C. jejuni gene shown to participate in longer term survival in epithelial cells. Comparing wt to the delta spoT mutant also revealed a strong correlation between gene expression profiles and phenotype differences observed. Together, these data demonstrate a critical role for the C. jejuni stringent response in multiple aspects of C. jejuni biology and pathogenesis.
2005-08-23 | E-SMDB-3292 | biostudies-arrayexpress
Project description:Campylobacter jejuni is a highly prevalent food-borne pathogen that causes diarrhoeal disease in humans. A natural zoonotic, it must overcome significant stresses both in vivo and during transmission despite the absence of several traditional stress response genes. Its ability to interact with and invade human intestinal epithelial cells closely correlates with virulence. A C. jejuni microarray-based screen revealed that several known virulence genes and several uncharacterized genes, including spoT, were rapidly upregulated during infection of human epithelial cells. spoT and its homologue relA have been shown in other bacteria to regulate the stringent response, an important stress response that to date had not been demonstrated for C. jejuni. We have found that C. jejuni mounts a stringent response that is regulated by spoT. Detailed analyses of a C. jejuni delta spoT mutant revealed that the stringent response is required for several specific stress, transmission and antibiotic resistance-related phenotypes. These include stationary phase survival, growth and survival under low CO2/high O2 conditions, and rifampicin resistance. A secondary suppressor strain that specifically rescues the low CO2 growth defect of the delta spoT mutant was also isolated. The stringent response additionally proved to be required for the virulence-related phenotypes of adherence, invasion, and intracellular survival in two human epithelial cell culture models of infection; spoT is the first C. jejuni gene shown to participate in longer term survival in epithelial cells. Comparing wt to the delta spoT mutant also revealed a strong correlation between gene expression profiles and phenotype differences observed. Together, these data demonstrate a critical role for the C. jejuni stringent response in multiple aspects of C. jejuni biology and pathogenesis. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set
2005-08-27 | GSE3209 | GEO
Project description:Campylobacter jejuni is a highly prevalent food-borne pathogen that causes diarrhoeal disease in humans. A natural zoonotic, it must overcome significant stresses both in vivo and during transmission despite the absence of several traditional stress response genes. Its ability to interact with and invade human intestinal epithelial cells closely correlates with virulence. A C. jejuni microarray-based screen revealed that several known virulence genes and several uncharacterized genes, including spoT, were rapidly upregulated during infection of human epithelial cells. spoT and its homologue relA have been shown in other bacteria to regulate the stringent response, an important stress response that to date had not been demonstrated for C. jejuni. We have found that C. jejuni mounts a stringent response that is regulated by spoT. Detailed analyses of a C. jejuni delta spoT mutant revealed that the stringent response is required for several specific stress, transmission and antibiotic resistance-related phenotypes. These include stationary phase survival, growth and survival under low CO2/high O2 conditions, and rifampicin resistance. A secondary suppressor strain that specifically rescues the low CO2 growth defect of the delta spoT mutant was also isolated. The stringent response additionally proved to be required for the virulence-related phenotypes of adherence, invasion, and intracellular survival in two human epithelial cell culture models of infection; spoT is the first C. jejuni gene shown to participate in longer term survival in epithelial cells. Comparing wt to the delta spoT mutant also revealed a strong correlation between gene expression profiles and phenotype differences observed. Together, these data demonstrate a critical role for the C. jejuni stringent response in multiple aspects of C. jejuni biology and pathogenesis. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Computed
2005-08-27 | E-GEOD-3209 | biostudies-arrayexpress
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:Objective: We previously showed that Campylobacter jejuni Cas9 was necessary for full virulence and efficient induction of human cell stress followed by cell death, but no virulence mechanism could be unravelled then. Therefore, we carried out global genome-wide transcriptomics, using RNA samples extracted from cells infected by a wild-type C. jejuni strain and the corresponding cas9 deletion strain. Methods: Caco-2 epithelial cells were infected with C. jejuni wild-type or cas9 deletion strains and RNA was extracted at 5 timepoints post-infection. Results: Wild-type C. jejuni induced cellular stress, DNA damage and cell death pathways in Caco-2 cells continuously from 30 min up to 4 hours after infection, eventually followed by visual cell death induction after 24 hours; the corresponding cas9 deletion strain did also induce cell stress pathways within the first two hours of infection but at later timepoints, stress pathway induction had dropped and after 4 hours of infection, expression of the corresponding stress genes had normalised to near-t=0 (uninfected) expression values; the cas9 deletion strain did not lead to visual cell death induction after 24 hours. Conclusions: Campylobacter jejuni Cas9 is necessary for full virulence of C. jejuni and is involved in the efficient induction of cellular stress pathways and eventually, cell death.
2018-09-30 | GSE89661 | GEO
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
Project description:Campylobacter jejuni is the leading bacterial cause of human gastroenteritis worldwide. Despite stringent microaerobic growth requirements, C. jejuni is ubiquitous in the aerobic environment. C. jejuni must possess finely tuned regulatory systems to sense and adapt to external stimuli such as oxidative and aerobic (O2) stress. Re-annotation of the C. jejuni NCTC11168 genome sequence identified Cj1556 (originally annotated as a hypothetical protein) as a MarR family transcriptional regulator and further bioinformatic analysis indicated a role in regulating the oxidative stress response. A C. jejuni 11168H Cj1556 mutant exhibited increased sensitivity to oxidative and aerobic stress, decreased ability for intracellular survival in both Caco-2 human intestinal epithelial cells and J774A.1 mouse macrophages and a reduction in virulence in the Galleria mellonella infection model. Microarray analysis of gene expression changes in the Cj1556 mutant compared to the wild-type strain indicated negative autoregulation of Cj1556 expression and down-regulation of genes associated with oxidative and aerobic stress responses, such as katA, perR and hspR. cprS, which encodes a sensor kinase involved in the regulation of biofilm formation, was also up-regulated in the Cj1556 mutant and subsequent studies showed that the Cj1556 mutant had a reduced ability to form biofilms. Protein interaction studies confirmed the binding of recombinant Cj1556 to a region upstream of Cj1556. This study has identified a novel C. jejuni transcriptional regulator Cj1556 that is involved in oxidative and aerobic stress responses and is important for the survival of C. jejuni in the natural environment and in vivo. This newly identified regulator was designated CosR (Campylobacter oxidative stress Regulator). Data is also available from <ahref=""http://bugs.sgul.ac.uk/E-BUGS-119"" target=""_blank"">BuG@Sbase</a>
2012-01-23 | E-BUGS-119 | biostudies-arrayexpress
Project description:DksA is well-known for its regulatory role in the transcription of ribosomal RNA and genes involved in amino acid synthesis in many bacteria. DksA is also reported to control expression of virulence genes in pathogenic bacteria. Here, we elucidated the roles of the DksA-like protein (CJJ81176_0160, Cj0125c) in the pathogenesis of Campylobacter jejuni. Like in other bacteria, transcription of stable RNA was repressed by DksA under stressful conditions in C. jejuni. Transcriptomic and proteomic analyses of C. jejuni 81-176 and its isogenic dksA mutant showed differential expression of many genes involved in iron-related metabolism, flagellar synthesis and amino acid metabolism. Also the dksA mutant of C. jejuni demonstrated a decreased ability to invade into intestinal cells and to induce release of interleukin-8 from intestinal cells. These results suggest the DksA-like protein plays an important regulatory role in the physiology and virulence of C. jejuni. Keywords: dksA mutation of Campylobacter jejuni
2008-05-06 | GSE9866 | GEO
Project description:C. jejuni, a spiral-shaped gram-negative bacterium, is a leading bacterial cause of human foodborne illness. Acute disease is associated with C. jejuni invasion of the intestinal epithelium. Further, maximal host cell invasion requires the secretion of proteins termed Campylobacter invasion antigens (Cia). As bile acids are known to alter the pathogenic behavior of other gastrointestinal pathogens, we hypothesized that the virulence potential of Campylobacter may be triggered by the bile acid deoxycholate (DOC). In support of this hypothesis, culturing C. jejuni with a physiologically relevant concentration of DOC significantly altered the kinetics of cell invasion as evidenced by gentamicin-protection assays. In contrast to C. jejuni harvested from Mueller-Hinton (MH) agar plates, C. jejuni harvested from MH agar plates supplemented with DOC demonstrated Cia secretion as judged by metabolic labeling experiments. DOC was also found to induce the expression of the ciaB gene as judged by B-galactosidase reporter assays and real-time RT-PCR. Microarray analysis revealed that DOC induced the expression of virulence genes (i.e., ciaB, cmeABC, dccR, and tlyA). In summary, we demonstrate that it is possible to enhance the pathogenic behavior of C. jejuni by modifying the culture conditions. These results provide a foundation to identify genes expressed by C. jejuni in response to in vivo-like culture conditions. Keywords: Stress response
2008-01-10 | GSE10110 | GEO
Project description:Campylobacter jejuni is a prevalent cause of bacterial gastroenteritis in humans worldwide. The mechanism by which C. jejuni survives stomach acidity remains unknown. Herein, we have demonstrated that C. jejuni with a fur deletion was more sensitive to acid than the wild-type strain. Profiling the acid stimulon of the C. jejuni ∆fur mutant allowed us to uncover Fur-regulated genes under acidic conditions. The up-regulation of heat shock genes and the down-regulation of genes involved in flagellar and cell envelope biogenesis in the fur mutant highlight the importance of Fur in Campylobacter acid survival. Interestingly, prior acid exposure of C. jejuni cross-protected the bacterium against oxidative stress. Western-blot analysis and real-time qRT-PCR revealed an increased expression of the catalase KatA in acid-stressed C. jejuni relative to unstressed bacteria. The enhanced survival of C. jejuni to oxidative stress was shown to be Fur-dependent through the regulation of katA expression. Electrophoretic mobility shift assay (EMSA) demonstrated that the binding affinity between Fur and katA is reduced under low pH allowing for higher expression of katA and the defense against oxidative stress. Strikingly, the ∆fur mutant exhibited a reduced virulence capacity in both human epithelial cells and G. mellonella infection model as compared to C. jejuni wild-type. Altogether, this is the first study showing that in addition to its role in iron metabolism, Fur is an important regulator of C. jejuni acid response and cross-protection against other stresses. Moreover, our results clearly demonstrate that Fur plays a substantial role in C. jejuni host pathogenesis. Campylobacter jejuni is a prevalent cause of bacterial gastroenteritis in humans worldwide. The mechanism by which C. jejuni survives stomach acidity remains unknown. Herein, we have demonstrated that C. jejuni with a fur deletion was more sensitive to acid than the wild-type strain. Profiling the acid stimulon of the C. jejuni ∆fur mutant allowed us to uncover Fur-regulated genes under acidic conditions. The up-regulation of heat shock genes and the down-regulation of genes involved in flagellar and cell envelope biogenesis in the fur mutant highlight the importance of Fur in Campylobacter acid survival. Interestingly, prior acid exposure of C. jejuni cross-protected the bacterium against oxidative stress. Western-blot analysis and real-time qRT-PCR revealed an increased expression of the catalase KatA in acid-stressed C. jejuni relative to unstressed bacteria. The enhanced survival of C. jejuni to oxidative stress was shown to be Fur-dependent through the regulation of katA expression. Electrophoretic mobility shift assay (EMSA) demonstrated that the binding affinity between Fur and katA is reduced under low pH allowing for higher expression of katA and the defense against oxidative stress. Strikingly, the ∆fur mutant exhibited a reduced virulence capacity in both human epithelial cells and G. mellonella infection model as compared to C. jejuni wild-type. Altogether, this is the first study showing that in addition to its role in iron metabolism, Fur is an important regulator of C. jejuni acid response and cross-protection against other stresses. Moreover, our results clearly demonstrate that Fur plays a substantial role in C. jejuni host pathogenesis.
2016-03-17 | GSE73796 | GEO