Vibrio Cholera from Bangladesh
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ABSTRACT:
PROVIDER: PRJEB18714 | ENA |
REPOSITORIES: ENA
Similar Datasets
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: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: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:All arrays used in Hyperinfectivity study Merrell DS, Butler SM, Qadri F, Dolganov NA, Alam A, Cohen MB, Calderwood SB, Schoolnik GK, Camilli A. Related Articles Host-induced epidemic spread of the cholera bacterium. Nature. 2002 Jun 6;417(6889):642-5. PMID: 12050664 A=patient A, B=patient B, C=patient C, stationary phase=stationary phase vibrio for comparison, and numbers represent technical replicates of the denoted sample.
2005-07-21 | E-SMDB-1384 | biostudies-arrayexpress
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:O139 serogroup from cholera outbreak in India and Bangladesh
| PRJNA15666 | ENA
Project description:Multi-isolate Vibrio cholera
| PRJNA59871 | ENA
Project description:Vibrio cholera CIRS 101 Genome sequencing
| PRJNA39603 | ENA
Project description: Not available
| S-EPMC1698305 | biostudies-literature