Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptional profiling of Campylobacter jejuni wild-type 81-176 and its ciprofloxacin-resistant derivative (P3) in the presence and absence of ciprofloxacin

ABSTRACT: Campylobacter jejuni is one of the most important zoonotic enteric bacterial pathogens able to colonize the gastrointestinal tract of various animals. The number of campylobacteriosis cases has increased worldwide and the particular concern has been the high level of fluoroquinolone resistance observed in C. jejuni isolates. In this study, we explored the effect of ciprofloxacin in Campylobacter jejuni by gene expression microarray analysis. The comparisons of transcriptional responses were performed in the absence and presence of ciprofloxacin with the wild-type strain 81-176 and its intermediate-resistant variant (P3). The resistant variant contained a single-nucleotide mutation causing amino acid change Asp-90-Asn in the gyrA gene instead of the most common Thr-86-Ile, causing a high-level resistance to ciprofloxacin. After the short-term exposure to a relatively high concentration of ciprofloxacin, the viability of C. jejuni 81-176 wild-type cells remained notably high when compared with other gram-negative bacteria. The general responses of short-term ciprofloxacin exposure were determined from both genetic backgrounds and resulted in the expression variation of genes participating in general cellular processes, e.g. , in carbon and amino-acid metabolism and protein transport. Ciprofloxacin effect for gene expression was measured from both genetic backgrounds after 1 hour exposure at the level of 0 and 8 Âµg/ml ciprofloxacin in MH-broth. For RNA isolation, 5 independent experiments with and without ciprofloxacin were performed, and 4 replicates of each total RNA was applied for the gene expression study.

ORGANISM(S): Campylobacter jejuni subsp. jejuni 81-176

SUBMITTER: Heidi HyytiÃ¤inen

PROVIDER: E-GEOD-41822 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

Dataset Information

Transcriptional profiling of Campylobacter jejuni wild-type 81-176 and its ciprofloxacin-resistant derivative (P3) in the presence and absence of ciprofloxacin

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