Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1161394 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Our data demonstrate the suitability of target capture technology for purifying very low quantities of Leptospira DNA from biological samples where the human genome is in vast excess. This enables deep sequencing of partial Leptospira genomes directly from clinical samples using next generation technologies and genotyping.
2022-05-23 | E-MTAB-11667 | biostudies-arrayexpress
Project description:Creation of a new library entries for Candida auris using MALDI Biotyper. Candida auris has a high genetic variability in the world, the identification of Colombian isolates is difficult using the main Bruker library. A new in-house library was created using Colombian isolated and was validated using 300 isolated strains
2020-06-02 | PXD016387 | Pride
Project description:Pathogenic Leptospira spp. are the causative agents of the zoonotic disease leptospirosis. During infection, Leptospira are confronted with deadly reactive oxygen species (ROS). Withstanding ROS produced by the host innate immunity is an important strategy evolved by pathogenic Leptospira for persisting in and colonizing hosts. The peroxide stress regulator, PerR, represses genes involved in ROS defenses in L. interrogans. We have performed RNA sequencing in WT and perR mutant strains to characterize the L. interrogans adaptive response to hydrogen peroxide. We showed that Leptospira solicit three main peroxidase machineries (catalase, cytochrome C peroxidase and peroxiredoxin) and heme to adapt to peroxide stress as well as canonical chaperones of the heat shock response, and DNA repair. Determining the PerR regulon allowed to identify the PerR-dependent mechanisms of the peroxide adaptive response and has revealed a regulatory network involving other transcriptional regulators, two-component systems and sigma factors as well as non-coding RNAs that putatively orchestrate, in concert with PerR, this adaptive response. Our findings provide comprehensive insight into the mechanisms required by pathogenic Leptospira to overcome infection-related oxidants. This will participate in framing future hypothesis-driven studies to identify and decipher novel virulence mechanisms.
2020-09-22 | GSE140019 | GEO
Project description:Mandatory potency testing of Leptospira vaccine batches relies partially on in vivo procedures, requiring large numbers of laboratory animals. Cell-based assays could replace in vivo tests if biomarkers indicative of Leptospira vaccine potency are identified. We investigated innate immune responsiveness induced by inactivated L. interrogans serogroups Canicola and Icterohaemorrhagiae, and two bivalent, non-adjuvanted canine Leptospira vaccines containing the same serogroups. First, the transcriptome and proteome analysis of canine 030-D cells stimulated with Leptospira strains, and the corresponding vaccine revealed more than 900 DEGs and 23 DEPs in common to these three stimuli. Second, comparison of responses induced by this Leptospira vaccine and a vaccine from another manufacturer revealed a large overlap in DEGs and DEPs as well, suggesting potential to identify biomarkers of Leptospira vaccine activity. Because not many common DEPs were identified, we selected seven molecules from the identified DEGs, associated with pathways related to innate immunity, of which CXCL-10, IL-1β, SAA, and complement C3 showed increased secretion upon stimulation with both Leptospira vaccines. These molecules could be interesting targets for development of biomarker-based assays in the future. Additionally, this study contributes to the understanding of the mechanisms by which Leptospira vaccines induce innate immune responses in the dog.
2022-03-06 | PXD031875 | Pride
Project description:Leptospirosis, caused by bacteria of the genus Leptospira, is a zoonotic disease affecting humans, companion animals, and all major livestock species. Typical propagation of the highly fastidious Leptospira borgepetesenii serovar Hardjo is limited to 29°C. However, newer culture media formulations now facilitate isolation and propagation at 37°C, a temperature that more closely emulates in vivo conditions and is hypothesized to regulate the expression of virulence factors during host infection. Since protein expression by leptospires is temperature dependent, and therefore the proteome of bacterin vaccines can differ whether grown at 37°C compared to 29°C, we compared the proteome of strains of Leptospira borgpetersenii serovar Hardjo at each temperature; two well-established strains that causes acute (strain JB197) or chronic asymptomatic disease (strain HB203) in the hamster challenge model of leptospirosis and two more recently isolated strains designated TC129 and TC273 (both of which cause chronic asymptomatic disease in the hamster). We found proteomic expression differences within strains propagated at the routine temperature of 29°C, and compared to the newly achieved culture temperature of 37°C. Results highlight significant differential protein expression, including virulence factors, amongst identical serovars of L. borgpetersenii when propagated at 29oC, the collective variation of which can be diminished when propagated at 37oC. Collectively, there is increasingly more evidence available to suggest bacterin vaccine design would benefit from consideration of strains employed, and potential effects of growth temperature related to specific behavior of pathogens in vaccine composition.
2022-05-20 | PXD032831 | Pride
Project description:The overall goal of these experiments was to determine how human endothelial cells respond to pathogenic Leptospira interrogans. Leptospira interrogans causes leptospirosis, the most widespread zoonotic infection in the world. A hallmark of leptospirosis is widespread endothelial damage, which in severe cases leads to hemorrhage. In these experiments, we infected two endothelial cell lines with pathogenic Leptospira interrogans serovar Canicola strain Ca12-005, and as controls, with the non-pathogenic Leptospira biflexa serovar Patoc strain Pfra. As additional controls, uninfected cells were also included in the analyses.
2010-07-27 | GSE23173 | GEO
Project description:The overall goal of these experiments was to determine how human endothelial cells respond to pathogenic Leptospira interrogans. Leptospira interrogans causes leptospirosis, the most widespread zoonotic infection in the world. A hallmark of leptospirosis is widespread endothelial damage, which in severe cases leads to hemorrhage. In these experiments, we infected two endothelial cell lines with pathogenic Leptospira interrogans serovar Canicola strain Ca12-005, and as controls, with the non-pathogenic Leptospira biflexa serovar Patoc strain Pfra. As additional controls, uninfected cells were also included in the analyses.
2010-07-27 | GSE23172 | GEO
Project description:Leptospirosis is a global zoonotic, neglected tropical disease. Interestingly, a high level of species specificity (both bacteria and host) plays a major role in the severity of disease presentation which can vary from asymptomatic to multi-organ failure. Pathogenic Leptospira colonize the kidneys of infected individuals and are shed in urine into the environment where they can survive until they are contracted by another host. This study looks at two strains of L. borgpetersenii, HB203 and JB197 which are genetically very similar, and identical by serotyping as serovar Hardjo, yet HB203 causes a chronic infection in the hamster while JB197 causes organ failure and mortality. To better characterize bacterial factors causing different disease outcomes, we examined the gene expression profile of these strains in the context of temperatures that would reflect natural Leptospira life cycles (environmentally similar 29oC and 37oC which is more indicative of host environment). We found vast differences in gene expression both between the strains and within strains between temperatures. Characterization of the transcriptome of L. borgpetersenii serovar Hardjo strains JB197 and HB203 provides insights into factors that can determine acute versus chronic disease in the hamster model of infection. Additionally, these studies highlight strain to strain variability within the same species, and serovar, at different growth temperatures, which needs to be considered when serovars are selected and propagated for use as bacterin vaccines used to immunize domestic animal species.
2021-04-28 | GSE168507 | GEO
Project description:The life-threatening pathogen Leptospira interrogans navigates a dual existence: surviving in environmental reservoirs and infecting mammalian hosts. Leptospira biofilm formation is thought to be an important survival strategy in environmental contexts and may also contribute to the persistence of leptospirosis in maintenance hosts. Examining the correlation between biofilm formation and the virulence of pathogenic strains might improve our comprehension of the epidemiology of leptospirosis. To further explore Leptospira’s survival strategy, our study focused on elucidating the biological state of pathogenic Leptospira within biofilms, particularly aiming to uncover the adaptations and regulatory mechanisms that are involved in such complex microenvironments. To determine the transcriptional profile of pathogenic Leptospira in biofilm, we compared the genome-wide transcriptomic profiles in late biofilms (21 days old) with those in exponential planktonic cultures (5 days old), revealing a pronounced transcriptomic shift. While genes linked to motility, energy production, and metabolism were downregulated, those governing the general stress response, defense against metal stress, and redox homeostasis showed a significant upsurge, hinting at a tailored defensive strategy against stress in late biofilms. A standout finding was the increased expression of the csoR, copZ, and copA locus, integral to copper ion stress response in other bacterial genera, suggesting a unique adaptation to metal-induced stress. Further, despite a reduced metabolic state in biofilms, their disruption swiftly restored metabolic activity. Crucially, bacteria either in late biofilms or resulting from biofilm disruption retained virulence in a hamster infection model, defying the notion that biofilm maturation abolishes pathogenicity. In summary, our study highlights Leptospira's adaptive equilibrium in biofilms: minimizing cellular energy expenditure to conserve resources, potentially aiding in withstanding stresses while maintaining its pathogenicity. These insights are important for explaining the survival strategies of Leptospira, revealing that a biofilm lifestyle may confer an advantage in maintaining virulence. This understanding is essential for managing leptospirosis across both environmental reservoirs and mammalian hosts.
2024-10-09 | GSE271193 | GEO