Members of the human gut microbiota involved in recovery from Vibrio cholerae infection
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ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| ERR520347.fastq.gz | Fastqsanger.gz | |||
| ERR520348.fastq.gz | Fastqsanger.gz | |||
| ERR520349.fastq.gz | Fastqsanger.gz | |||
| ERR520350.fastq.gz | Fastqsanger.gz |
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Project description:Understanding gene expression by bacteria during the actual course of human infection may provide important insights into microbial pathogenesis. In this study, we evaluated the transcriptional profile of Vibrio cholerae, the causative agent of cholera, in clinical specimens from cholera patients. We collected samples of human stool and vomitus that were positive by dark-field microscopy for abundant vibrios and used a microarray to compare gene expression in organisms recovered directly from the early and late stages of human infection. Our results reveal that V. cholerae gene expression within the human host environment differs from patterns defined in in vitro models of pathogenesis. tcpA, the major subunit of the essential V. cholerae colonization factor, was significantly more highly expressed in early compared with late infection; however, the genes encoding cholera toxin were not highly expressed in either phase of human infection. Furthermore, expression of the virulence regulators, toxRS and tcpPH, was uncoupled. Interestingly, the pattern of gene expression indicates that the human upper intestine may be a uniquely suitable environment for the transfer of genetic elements that are important in the evolution of pathogenic strains of V. cholerae. These findings provide a more detailed assessment of the transcriptome of V. cholerae in the human host than previous studies of organisms in stool alone and have implications for cholera control and the design of improved vaccines. Keywords: comparative gene expression analysis
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Project description:Understanding gene expression by bacteria during the actual course of human infection may provide important insights into microbial pathogenesis. In this study, we evaluated the transcriptional profile of Vibrio cholerae, the causative agent of cholera, in clinical specimens from cholera patients. We collected samples of human stool and vomitus that were positive by dark-field microscopy for abundant vibrios and used a microarray to compare gene expression in organisms recovered directly from the early and late stages of human infection. Our results reveal that V. cholerae gene expression within the human host environment differs from patterns defined in in vitro models of pathogenesis. tcpA, the major subunit of the essential V. cholerae colonization factor, was significantly more highly expressed in early compared with late infection; however, the genes encoding cholera toxin were not highly expressed in either phase of human infection. Furthermore, expression of the virulence regulators, toxRS and tcpPH, was uncoupled. Interestingly, the pattern of gene expression indicates that the human upper intestine may be a uniquely suitable environment for the transfer of genetic elements that are important in the evolution of pathogenic strains of V. cholerae. These findings provide a more detailed assessment of the transcriptome of V. cholerae in the human host than previous studies of organisms in stool alone and have implications for cholera control and the design of improved vaccines. The V. cholerae microarray consists of 3,890 full-length PCR products representing the annotated open reading frames from the initial release of the V. cholerae N16961 genome. Each labeling and hybridization was performed in duplicate. Genomic DNA was used as a universal internal control for the quality of the microarray and to allow for the comparison of results across multiple experiments. Data were normalized using locally-weighted regression (Lowess) to obtain the relative abundance of each transcript as an intensity ratio with respect to that of genomic DNA. High correlation coefficients were observed between technical replicates (Pearsonâs correlation coefficient (r) > 0.80) and between results of separate clinical specimens of vomitus (r > 0.77) and of stool (r > 0.80). Hence, the results from the two clinical vomitus specimens and the five clinical stool specimens were pooled. Fold changes for the relative expression of a given gene between the two clinical specimens were calculated by dividing the normalized median intensity ratios with respect to genomic DNA.
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Project description:Vibrio cholerae is a Gram negative, motile, facultative anaerobic bacterium, and the causative agent of cholera, a severe diarrhoeal disease, which untreated can rapidly lead to dehydration, hypotensive shock, and death. Cholera is a significant human disease that is estimated to affect 3-5 million people each year. The mechanism by which V. cholerae regulates virulence gene expression in vivo is unknown, but a number of studies have suggested that low molecular weight signally molecules may be important in modulating gene expression. cFP is a low molecular weight cyclic dipeptide produced by multiple Vibrio species. Evidence previously generated in our laboratory showed that cFP inhibited the production of the virulence factors cholera toxin (CT) and the toxin coregulated pilus (TCP) in O1 El Tor V. cholerae strain N16961 during growth under virulence gene inducing conditions. cFP inhibition of CT and TCP production correlated with reduced transcription of several regulators that belong to the ToxR regulon. To identify additional cFP-responsive genes we performed microarray experiments with the O1 El Tor V. cholerae strain N16961. In these experiments N16961 was grown under virulence gene inducing conditions in the presence and absence of cFP before RNA was extracted and hybridized to microarrays. The results showed that cFP positively affected the expression of the LysR-family regulatory protein LeuO. This finding suggests the possibility that LeuO may be mediating cFP-dependent regulation of gene expression in response to environmental cFP. V. cholerae N16961 was grown under AKI growth condition in the presence or absence of 1 mM cFP for 2.5 or 3 hours when total RNA was extracted, differentially labelled and hybridized to microarrays. Four independent experiments were performed.
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