Rickettsia conorii
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA35061 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Causative agent for Rocky Mountain Spotted Fever
| PRJNA17833 | ENA
Project description:Obligate intracellular pathogen that causes Rocky Mountain Spotted Fever
| PRJNA42 | ENA
Project description:Strains of R. rickettsii, the agent of Rocky Mountain spotted fever, differ greatly in the severity of the disease caused. The genetic differences responsible for this disparity are only now being uncovered. An avirulent, laboratory adapted strain of R. rickettsii fails to proteolytically process several large surface protein antigens. We have identified a protease that cleaves the protein precursors to their mature form. The gene encoding this protease is mutated in the avirulent strain. Complementation of the active form of the gene identifies proteolytic processing of surface antigens as important to virulence.
2023-07-06 | PXD041355 | Pride
Project description:Obligate intracellular pathogen that causes Rocky Mountain Spotted Fever
| PRJNA19943 | ENA
Project description:Obligate intracellular pathogen that causes Rocky Mountain Spotted Fever
| PRJNA9636 | ENA
Project description:Rickettsia conorii is the etiologic agent of Mediterranean spotted fever, a re-emerging disease with significant mortality. This obligate, gram-negative intracellular pathogen is transmitted via tick bites, resulting in disseminated vascular endothelial cell infection with vascular leakage. In the infected human, Rickettsia conorii infects endothelial cells, stimulating expression of cytokines and pro-coagulant factors. However, the integrated proteomic response of human endothelial cells to R. conorii infection is not known. In this study, we performed quantitative proteomic profiling of R conorii –infected primary HUVECs vs those stimulated with LPS alone.
2015-11-17 | PXD002650 | Pride
Project description:Rickettsia conorii is the etiologic agent of Mediterranean spotted fever, a re-emerging disease with significant mortality. This obligate, gram-negative intracellular pathogen is transmitted via tick bites, resulting in disseminated vascular endothelial cell infection with vascular leakage. In the infected human, Rickettsia conorii infects endothelial cells, stimulating expression of cytokines and pro-coagulant factors. However, the integrated proteomic response of human endothelial cells to R. conorii infection is not known. In this study, we performed quantitative proteomic profiling of R conorii â??infected primary HUVECs vs those stimulated with LPS alone.
2017-04-01 | MSV000080856 | MassIVE
Project description:The causal agent of Oriental Spotted Fever
| PRJNA38529 | ENA
Project description:Different types of cell death, including apoptosis, play an important role in the immune defense of arthropods, as infected cells are eliminated, preventing the dissemination of the infectious agent throughout the animal body. The apoptosis can be triggered by two main pathways: the intrinsic or mitochondrial pathway and the extrinsic or death receptor pathway. Both culminate in the activation of the effector caspases, such as caspase-3, resulting, for instance in DNA fragmentation and exposition of markers on the surface of the apoptotic cell, allowing its recognition and elimination by phagocytic cells. To ensure survival and proliferation, microorganisms can inhibit apoptosis of the host cell. The differential proteome of a tick cell line (BME26) in response to an experimental infection with Rickettsia rickettsii, causative agent of the severe Rocky Mountain spotted fever, showed that pro-apoptotic proteins are downregulated in the beginning of infection (6 h) and upregulated in a later time-point (48 h). We therefore evaluated the effects of infection on classic features of apoptotic cells: the spontaneous fragmentation of gDNA and the activity of caspase-3 and the exposition of phosphatidylserine in BME26 cells after induction with staurosporine, a classic activator of apoptosis. The spontaneous fragmentation of DNA was observed exclusively in non-infected cells. In addition, the activity of caspase-3 and the exposition of phosphatidylserine is lower in infected than in non-infected cells. Caspase-3 activity is also lower in infected IBU/ASE-16 cells, an embryonic tick cell line of one primary vector of R. rickettsii in Brazil, Amblyomma sculptum. Importantly, while the activation of caspase-3 exerted a detrimental effect on rickettsial proliferation in BME26 cells, the enzyme inhibition increased bacterial growth. Together, our results suggest that R. rickettsii controls the apoptosis in tick cells, which seems to be important to ensure the colonization of the vector cell. To the best of our knowledge, this is the first report on the modulation of the apoptosis in a tick cell line upon the infection with a species of the genus Rickettsia.
2021-09-09 | PXD017942 | Pride
Project description:Rickettsiae are strict obligate intracellular pathogens that alternate between arthropod and mammalian hosts in a zoonotic cycle. Typically, pathogenic bacteria that cycle between environmental sources and mammalian hosts adapt to the respective environments by coordinately regulating gene expression such that genes essential for survival and virulence are expressed only upon infection of mammals. Temperature is a common environmental signal for upregulation of virulence gene expression although other factors may also play a role. We examined the transcriptional responses of Rickettsia rickettsii, the agent of Rocky Mountain spotted fever, to a variety of environmental signals expected to be encountered during its life cycle. R. rickettsii exposed to differences in growth temperature (25o C vs. 37o C), iron limitation, and host cell species displayed nominal changes in gene expression under any of these conditions with only 0, 5, or 7 genes, respectively, changing more than 3-fold in expression levels. R. rickettsii is not totally devoid of ability to respond to temperature shifts as cold shock (37o C vs. 4o C) induced a change greater than 3-fold in up to 57 genes. Rickettsiae continuously occupy a relatively stable environment which is the cytosol of eukaryotic cells. Because of their obligate intracellular character, rickettsiae are believed to be undergoing reductive evolution to a minimal genome. We propose that their relatively constant environmental niche has led to a minimal requirement for R. rickettsii to respond to environmental changes with a consequent deletion of non-essential transcriptional response regulators. A minimal number of transcriptional regulators in the R. rickettsii genome is consistent with this hypothesis.
2009-05-23 | GSE14965 | GEO