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PROVIDER: PRJNA497771 | ENA |
REPOSITORIES: ENA
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Project description:Temperature is a crucial environmental signal that govers the occurrence of Vibrio cholerae and cholera outbreaks. To understand how temperature impacts the transcriptome of V. cholerae we performed whole-genome level transcriptional profiling using custom microarrays on cells grown at human body temperature (37 C) then shifted to temperatures V. cholerae experience in the environment (15 C and 25 C).
2016-05-09 | GSE81158 | GEO
Project description:Pandemic and endemic strains of Vibrio cholerae arise from toxigenic conversion by the CTXφ bacteriophage, a process by which CTXφ infects non-toxigenic strains of V. cholerae. CTXφ encodes the cholera toxin, an enterotoxin responsible for the watery diarrhea associated with cholera infections. Despite the critical role of CTXφ during infections, signals that affect CTXφ-driven toxigenic conversion or expression of the CTXφ-encoded cholera toxin remain poorly characterized, particularly in the context of the gut mucosa. Here, we identify mucin polymers as potent regulators of CTXφ-driven pathogenicity in V. cholerae. Our results indicate that mucin-associated O-glycans block toxigenic conversion by CTXφ and suppress the expression of CTXφ-related virulence factors, including the toxin co-regulated pilus and cholera toxin, by interfering with the TcpP/ToxR/ToxT virulence pathway. By synthesizing individual mucin glycan structures de novo, we identify the Core 2 motif as the critical structure governing this virulence attenuation. Overall, our results highlight a novel mechanism by which mucins and their associated O-glycan structures affect CTXφ-mediated evolution and pathogenicity of V. cholerae, underscoring the potential regulatory power housed within mucus.
2022-12-01 | GSE213598 | GEO
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
2005-08-17 | GSE2775 | GEO
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.
2013-08-13 | GSE38272 | GEO
Project description:Antibodies targeting the O-specific polysaccharide (OSP) of Vibrio cholerae O1 are a main determinant of protection against cholera. These antibodies can agglutinate bacteria, and can also directly inhibit V. cholerae motility, including at sub-agglutinating conditions. In order to evaluate for possible additional impacts of OSP-specific antibody on V. cholerae, we assessed the transcriptional profile of V. cholerae exposed to an anti-OSP human monoclonal antibody (G1), including in the presence of mucin, the principal component of intestinal mucous. We identified a subset of genes whose expression was significantly altered in the presence of anti-OSP antibody and mucin, including those involved in V. cholerae metabolism, transport, stress response, biofilm formation, motility, and secondary messenger signaling. Our results suggest a broad impact of anti-OSP antibodies on V. cholerae in the presence of mucin and identify several possible mechanisms by which anti-OSP antibodies might protect against cholera.
2025-02-10 | GSE287993 | GEO
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.
2013-08-13 | E-GEOD-38272 | biostudies-arrayexpress
Project description:Activity-based protein profiling (ABPP) is a chemoproteomic tool for detecting active enzymes in complex biological systems. We used ABPP to identify secreted bacterial and host serine hydrolases that are active in animals infected with the cholera pathogen Vibrio cholerae. Four V. cholerae proteases were consistently active in infected rabbits, and one, VC0157 (renamed IvaP), was also active in human cholera stool. Inactivation of IvaP influenced the activity of other secreted V. cholerae and rabbit enzymes in vivo, while genetic disruption of all four proteases increased the abundance and binding of an intestinal lectin—intelectin—to V. cholerae in infected rabbits. Intelectin also bound to other enteric bacterial pathogens, suggesting it may constitute a previously unrecognized mechanism of bacterial surveillance in the intestine that is inhibited by pathogen-secreted proteases. Our work demonstrates the power of activity-based proteomics to reveal host-pathogen enzymatic dialogue in an animal model of infection.
2016-02-22 | PXD003000 | Pride
Project description:Horizontally acquired genetic elements (HGEs) plays a major for determination of virulence, antimicrobial resistance, adaptation and evolution in pathogenic bacteria. Conserved integrative mobile genetic elements (MGEs) of Vibrio cholerae contribute in the disease development, antimicrobial resistance and metabolic functions. To understand the dynamics of integrative MGEs and cross talk between MGEs and core genome, engineered genome of V. cholerae was monitored in the presence and absence of horizontally acquired genetic elements. Deletion of more than 250 revealed that CTX contributes to the essentiality of SOS response master regulator LexA in V. cholerae. Also, he core genome encoded RecA helps CTX to bypass the host immunity and replicate in the host cell in the presence of similar prophage in the host chromosome. Finally, our multiomics data reveal importance of MGEs in modulating the level of cellular proteome and metabolome in V. cholerae. This study for the first time engineered the genome of V. cholerae strains to eliminate all the GIs, ICE and prophages from their genome and revealed new interactions between core and acquired genomes. The engineered strain could be a potential candidate for understanding evolution of cholera pathogen and development of therapeutics.
2020-09-28 | PXD017801 | Pride
Project description:Vibrio cholerae, the cause of cholera, can grow in a variety of environments outside of human hosts. During infection, the pathogen must adapt to significant environmental alterations, including the elevated temperature of the human gastrointestinal tract. σ32, an alternative sigma factor encoded by rpoH, activates transcription of genes involved in the heat-shock response in several bacterial species. We defined the V. cholerae RpoH regulon by comparing the whole genome transcription profiles of the wild-type and rpoH mutant strains after a temperature up-shift. Most of the V. cholerae genes expressed in an RpoH-dependent manner after heat-shock encode proteins that influence protein fate, such as proteases and chaperones, or are of unknown function. Keywords: heat-shock response, rpoH
2007-01-03 | GSE6097 | GEO