Gene Expression Changes in Campylobacter jejuni triggered by exposure to Novobiocin
Ontology highlight
ABSTRACT:
ORGANISM(S): Campylobacter jejuni
PROVIDER: GSE18415 | GEO | 2009/12/28
SECONDARY ACCESSION(S): PRJNA118207
REPOSITORIES: GEO
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Project description:In order to investigate the gene experssion changes in Campylobacter jejuni triggered by exposure to Novobiocin. DNA microarray was used to identify genes that were differentially expressed in C. jejuni 11168 treated with Novobiocin. For RNA extraction, Campylobacter cells were grown 4 hrs in MH broth to the mid exponential phase (OD600=0.4-0.5) with shaking rates 180rpm at 42°C, and then split into two equal portions, one of which was treated with subinhibitory dose of Novobiocin (256ug/ml, 0.25 MIC) and the other served as a non-treated control, all of these samples were incubated at 42°C for 30 min under microaerobic conditions, RNA samples were extracted from 4 independent treatments and 4 non-treated controls. Then cDNA was synthesized using aminoallyl-dNTP and RNA samples according to the manufacturerâs instruction. After purification, aminoallyl labeled cDNA was fluorescently labeled with Cy-3/Cy-5 mono-Reactive Dye Pack.
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Project description:Gene Expression Changes in Campylobacter jejuni triggered by exposure to Novobiocin
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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.
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