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The microbiota conditions a gut-milieu which selects for wild-type Salmonella Typhimurium virulence

ABSTRACT: The microbiota conditions a gut-milieu which selects for wild-type Salmonella Typhimurium virulence

PROVIDER: PRJEB64217 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR11685700_1.fastq.gz	Fastqsanger.gz
	ERR11685700_2.fastq.gz	Fastqsanger.gz
	ERR11686000_1.fastq.gz	Fastqsanger.gz
	ERR11686000_2.fastq.gz	Fastqsanger.gz
	ERR11686100_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

The microbiota conditions a gut milieu that selects for wild-type Salmonella Typhimurium virulence.

Project description:Salmonella Typhimurium elicits gut inflammation by the costly expression of HilD-controlled virulence factors. This inflammation alleviates colonization resistance (CR) mediated by the microbiota and thereby promotes pathogen blooms. However, the inflamed gut-milieu can also select for hilD mutants, which cannot elicit or maintain inflammation, therefore causing a loss of the pathogen's virulence. This raises the question of which conditions support the maintenance of virulence in S. Typhimurium. Indeed, it remains unclear why the wild-type hilD allele is dominant among natural isolates. Here, we show that microbiota transfer from uninfected or recovered hosts leads to rapid clearance of hilD mutants that feature attenuated virulence, and thereby contributes to the preservation of the virulent S. Typhimurium genotype. Using mouse models featuring a range of microbiota compositions and antibiotic- or inflammation-inflicted microbiota disruptions, we found that irreversible disruption of the microbiota leads to the accumulation of hilD mutants. In contrast, in models with a transient microbiota disruption, selection for hilD mutants was prevented by the regrowing microbiota community dominated by Lachnospirales and Oscillospirales. Strikingly, even after an irreversible microbiota disruption, microbiota transfer from uninfected donors prevented the rise of hilD mutants. Our results establish that robust S. Typhimurium gut colonization hinges on optimizing its manipulation of the host: A transient and tempered microbiota perturbation is favorable for the pathogen to both flourish in the inflamed gut and also minimize loss of virulence. Moreover, besides conferring CR, the microbiota may have the additional consequence of maintaining costly enteropathogen virulence mechanisms.

| S-EPMC10499267 | biostudies-literature

Salmonella Modulates Metabolism during Growth under Conditions that Induce Expression of Virulence Genes

Project description:Salmonella enterica serovar Typhimurium (S. Typhimurium) is a facultative pathogen that uses complex mechanisms to invade and proliferate within mammalian host cells. To investigate possible contributions of metabolic processes to virulence in S. Typhimurium grown under conditions known to induce expression of virulence genes, we used a metabolomics-driven systems biology approach coupled with genome scale modeling. First, we identified distinct metabolite profiles associated with bacteria grown in either rich or virulence-inducing media and report the most comprehensive coverage of the S. Typhimurium metabolome to date. Second, we applied an omics-informed genome scale modeling analysis of the functional consequences of adaptive alterations in S. Typhimurium metabolism during growth under our conditions. Modeling efforts highlighted a decreased cellular capability to both produce and utilize intracellular amino acids during stationary phase culture in virulence conditions, despite significant abundance increases for these molecules as observed by our metabolomics measurements. Furthermore, analyses of omics data in the context of the metabolic model indicated rewiring of the metabolic network to support pathways associated with virulence. For example, cellular concentrations of polyamines were perturbed, as well as the predicted capacity for secretion and uptake.

2013-05-02 | MTBLS35 | MetaboLights

Effect of ppGpp on Salmonella Typhimurium gene expression

Project description:The expression profile of an S. Typhimurium mutant strain unable to synthesise ppGpp (relAspoT deletions) was compared to the wild-type strain. The effect of ppGpp on virulence gene expression was studied under 4 different growth conditions that induce virulence gene expression. Keywords: genetic modification

2006-05-30 | GSE4631 | GEO

FNR- vs WT in anoxic conditions

Project description:Salmonella enterica var. Typhimurium (S. Typhimurium) is a Gram-negative, facultative intracellular pathogen that infects the intestinal tracts of humans and animals. In the host, S. Typhimurium encounters a wide range of oxygen concentrations going from oxic conditions in the stomach to near anoxic conditions in the distal sigmoid colon-rectal junction. In Escherichia coli, FNR (Fumarate Nitrate Reductase) is one of the main regulatory proteins involved in oxygen sensing and in controlling the transcription of the genes required for the aerobic/anaerobic transition.. However, the role of FNR in S. Typhimurium is largely unknown. To assess its role in S. Typhimurium, we constructed an FNR- mutant (NC983) in the pathogenic wild-type (WT) strain, ATCC14028s. Keywords: FNR, Salmonella, anaerobic, virulence

2007-01-05 | GSE3657 | GEO

Mucispirillum schaedleri interferes with Salmonella Typhimurium virulence factor expression

Project description:Mucispirillum schaedleri interferes with Salmonella Typhimurium virulence factor expression

| PRJNA504618 | ENA

NIAID bacterial proteomes - Analysis of the Salmonella typhimurium proteome through environmental response toward infectious conditions

Project description:Analysis of the Salmonella typhimurium proteome through environmental response toward infectious conditions

2008-05-21 | PRD000057 | Pride

Expression analysis of Salmonella enterica serovar Typhimurium UK1 delta-iacP mutant

Project description:Investigation of whole genome gene expression level changes in a Salmonella enterica serovar Typhimurium UK1 delta-iacP mutant, compared to the wild-type strain. IacP is resoponsible for the secretion of virulence effector proteins via the type III secretion system, thereby contributing the virulence of S. Typhimurium. The mutants analyzed in this study are further described in Kim et al. 2011. Role of Salmonella Pathogenicity Island 1 Protein IacP in Salmonella enterica Serovar Typhimurium Pathogenesis. Infection and Immunity 79(4):1440-1450 (PMID 21263021).

2012-04-30 | GSE34663 | GEO

Salmonella Typhimurium reprograms macrophage metabolism via T3SS effector SopE2 to promote intracellular replication and virulence

Project description:Salmonella Typhimurium establishes systemic infection by replicating in host macrophages. Here we show that macrophages infected with S. Typhimurium exhibit upregulated glycolysis and decreased serine synthesis, leading to accumulation of glycolytic intermediates. The effects on serine synthesis are mediated by bacterial protein SopE2, a type III secretion system (T3SS) effector encoded in pathogenicity island SPI-1. The changes in host metabolism promote intracellular replication of S. Typhimurium via two mechanisms: decreased glucose levels lead to upregulated bacterial uptake of 2- and 3-phosphoglycerate and phosphoenolpyruvate (carbon sources), while increased pyruvate and lactate levels induce upregulation of another pathogenicity island, SPI-2, known to encode virulence factors. Pharmacological or genetic inhibition of host glycolysis, activation of host serine synthesis, or deletion of either the bacterial transport or signal sensor systems for those host glycolytic intermediates impairs S. Typhimurium replication or virulence.

2024-05-22 | MTBLS2347 | MetaboLights

General response of Salmonella enterica serovar Typhimurium to desiccation: A new role for the virulence factors sopD and sseD in survival.

Project description:Salmonella can survive for long periods under extreme desiccation conditions. This stress response poses a risk for food safety, but relatively little is known about the molecular and cellular regulation of this adaptation mechanism. To determine the genetic components involved in Salmonella’s cellular response to desiccation, we performed a global transcriptomic analysis comparing Salmonella Typhimurium cells equilibrated to low water activity (aw 0.11) and cells equilibrated to high water activity (aw 1.0). The analysis revealed that 719 genes were differentially regulated between the two conditions, of which 290 genes were up-regulated at aw 0.11. Most of these genes were involved in metabolic pathways, transporter regulation, DNA replication/repair, transcription and translation, and, more importantly, virulence genes.

2017-10-26 | GSE86580 | GEO

Mapping the Regulatory Network for Salmonella Typhimurium Invasion

Project description:Using RNAseq, the goal of the study is to investigate transcription factor regulation of virulence genes in 14028s Salmonella Typhimurium grown in SPI-1-inducing conditions. Transcription factors were cloned into pBAD24. RNA levels were compared in 14028s Salmonella Typhimurium with the transcription factor-encoding gene deleted, carrying either empty pBAD24, or pBAD24 expressing the transcription factor corresponding to the deletion. The Transcription factors analyzed are HilA, HilC, HilD, SprB, InvF, RtsA and RtsB.

2015-08-17 | E-MTAB-3765 | biostudies-arrayexpress

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