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ABSTRACT:
PROVIDER: PRJNA110527 | ENA |
REPOSITORIES: ENA
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Project description:HilD is a regulator of Salmonella pathogenicity island 1 (SPI-1) virulence genes in Salmonella enterica serovar Typhimurium. To identify novel HilD-regulated genes, we mapped the genome-wide association of HilD in S. Typhimurium under SPI-1-inducing conditions (high salt, low aeration) using ChIP-seq. HilD was C-terminally tagged with 3 FLAG tags in strain 14028s.
2013-09-19 | E-MTAB-1848 | biostudies-arrayexpress
Project description:Bacterial genotoxins, produced by several Gram-negative bacteria, induce DNA damage in the target cells. While the responses induced in the host cells have been extensively studied in vitro, the role of the genotoxins as effectors during the course of acute and chronic infections remains poorly characterized.To address this issue, we assessed the effects of the Salmonella enterica genotoxin, known as typhoid toxin, in in vivo models of murine chronic infections. Immunocompetent mice were chronically infected with isogenic S. enterica, serovar Typhimurium (S. Typhimurium) strains, encoding either a functional (MC71-TT) or an inactive (MC71-DcdtB) typhoid toxin. Keywords: salmonella typhimurium, bacterial genotoxins, typhoid toxin, chronic infection, mice model
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Project description:Profiling of mucosal derived bovine ab and gd T cells during Salmonella enterica serovar typhimurium enterocolitis
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Project description:In the context of host-pathogen interactions, gram-negative bacterial virulence factors, such as effectors, may be transferred from bacterial to eukaryotic host cytoplasm by multicomponent Type III protein secretion systems (T3SSs). Central to Salmonella enterica serovar Typhimurium (S. Typhimurium) pathogenesis is the secretion of over 40 effectors by two T3SSs encoded within pathogenicity islands SPI-1 and SPI-2. These effectors manipulate miscellaneous host cellular processes, such as cytoskeleton organization and immune signaling pathways, thereby permitting host colonization and bacterial dissemination. Recent research on effector biology provided mechanistic insights for some effectors. However, for many effectors, clearly defined roles and host target repertoires—further clarifying effector interconnectivity and virulence networks—are yet to be uncovered. Here we demonstrate the utility of the recently described viral-like particle trapping technology Virotrap as an effective approach to catalogue S. Typhimurium effector-host protein complexes (EH-PCs). Mass spectrometry-based Virotrap analysis of the novel E3 ubiquitin ligase SspH2 previously shown to be implicated in modulating actin dynamics and immune signaling, exposed known host interactors PFN1 and -2 and several putative novel, interconnected host targets. Network analysis revealed an actin(-binding) cluster among the significantly enriched hits for SspH2, consistent with the known localization of the S-palmitoylated effector with actin cytoskeleton components in the host. We show that Virotrap complements the current state-of-the-art toolkit to study protein complexes and represents a valuable means to screen for effector host targets in a high-throughput manner, thereby bridging the knowledge gap between effector-host interplay and pathogenesis.
2022-02-17 | PXD026740 | Pride
Project description:To cause disease, Salmonella enterica serovar Typhimurium requires two type-III secretion systems, encoded on Salmonella Pathogenicity Islands 1 and 2 (SPI-1 and -2). These secretion systems serve to deliver virulence proteins, termed effectors, into the host cell cytosol. While the importance of these effector proteins to promote colonization and replication within the host has been established, the specific roles of individual secreted effectors in the disease process are not well understood. In this study, we used an in vivo gallbladder epithelial cell infection model to study the function of the SPI-2-encoded effector, SseL. Deletion of the sseL gene resulted in bacterial filamentation and elongation and unusual localization of Salmonella within infected epithelial cells. Infection with the ΔsseL strain also caused dramatic changes in lipid metabolism and led to massive accumulation of lipid droplets in infected cells. Some of these changes were investigated through metabolomics of gallbladder tissue. This phenotype was directly attributed to the deubiquitinase activity of SseL, as a Salmonella strain carrying a single point mutation in the catalytic cysteine resulted in the same phenotype as the deletion mutant. Excessive buildup of lipids due to the absence of a functional sseL gene was also observed in S. Typhimurium-infected livers. These results demonstrate that SseL alters host lipid metabolism in infected epithelial cells by modifying ubiquitination patterns of cellular targets.
2011-08-23 | GSE27604 | GEO
Project description:Salmonella enterica serovar Typhimurium is a rod-shaped Gram-negative bacterium. It is a leading cause of gastroenteritis and public health problem. In the environment, it interacts with protozoa, particular amoeba, however the interactions between Salmonella and these eukaryotic microbes have not been addressed in detail. We and others recently described that S. Typhimurium is able to survive in the model amoeba Dictyostelium discoideum requiring the Salmonella pathogenicity islands 1 and 2 (SPI-1 and SPI-2, respectively)-encoded type three secretion systems (T3SSs). In this work, we investigated the role of two particular effector proteins, SopB and SifA that are secreted by either one of the T3SSs. SopB and SifA are involved in the remodelling of the intracellular compartment that contains Salmonella (Salmonella-containing vacuole, SCV) in other cellular models. We combined genetic and proteomics analysis to investigate the roles of SopB and SifA during infections of D. discoideum. We identified over 1,000 proteins per sample performing proteomics on fractions enriched in SCVs from amoeba cells infected with wild-type, sopB or sifA S. Typhimurium. Among them, we observed several Rho GTPases, guanine nucleotide exchange factors and motor proteins. Finally, we decided to evaluate if the changes observed in the proteome from the SCV of wild-type and mutants affect the intracellular survival of S. Typhimurium. These finding suggest that Salmonella exploits this route to survive intracellularly, a process that requires SopB and/or SifA effectors. To our knowledge this is the first proteomic description of the Salmonella intracellular compartment in D. discoideum.
2020-09-23 | PXD014955 | Pride