Defining stationary phase transcriptomes of Campylobacter jejuni cell morphotypes II
Ontology highlight
ABSTRACT:
ORGANISM(S): Campylobacter jejuni
PROVIDER: GSE116814 | GEO | 2018/07/10
REPOSITORIES: GEO
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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
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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 The design utilized a commercially available two color microarray slide for the enture transcriptome of Campylobacter jejuni. Six hybridizations were performed each with independently extracted samples of either C. jejuni wildtype of C. jejuni dksA mutant cDNA samples. A dye swap was utilized to help minimize dye dependent bias. Thus there were six biological replicates of each sample.
2008-05-05 | E-GEOD-9866 | 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
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:Expression arrays comparing Campylobacter jejuni NCTC11168 during growth in the cecum of germ-free C57 BL/6 IL-10 knockout mice to C. jejuni NCTC11168 during growth in Bolton broth.
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Project description:Defining stationary phase transcriptomes of Campylobacter jejuni cell morphotypes
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Project description:Campylobacter jejuni is a major zoonotic pathogen transmitted to humans via the food chain. C. jejuni is prevalent in chickens, a natural reservoir for this pathogenic organism. Due to the importance of macrolide antibiotics in clinical therapy of human campylobacteriosis, development of macrolide resistance in Campylobacter has become a concern for public health.To facilitate understanding the molecular basis associated with the fitness difference between Erys and Eryr Campylobacter, we compared the transcriptomes between ATCC 700819 and its isogenic Eryr transformant T.L.101 using DNA microarray.
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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