Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Nutritional immunity promotes intracellular survival of nontypeable Haemophilus influenzae

ABSTRACT: Nutritional immunity promotes intracellular survival of nontypeable Haemophilus influenzae via altered intracellular trafficking

INSTRUMENT(S): Q Exactive

ORGANISM(S): Haemophilus Influenzae (ncbitaxon:727)

SUBMITTER: Dr. J. Will Thompson Kevin M. Mason

PROVIDER: MSV000082399 | MassIVE | Thu May 24 10:38:00 BST 2018

REPOSITORIES: MassIVE

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Host metabolic reprogramming during immune activation promotes intracellular bacterial survival (2DG)

Project description:Host metabolic reprogramming during immune activation promotes intracellular bacterial survival (2DG)

| PRJNA578745 | ENA

Host metabolic reprogramming during immune activation promotes intracellular bacterial survival (host and bacteria)

Project description:Host metabolic reprogramming during immune activation promotes intracellular bacterial survival (host and bacteria)

| PRJNA578744 | ENA

Host metabolic reprogramming during immune activation promotes intracellular bacterial survival (glycerol or succinate)

Project description:Host metabolic reprogramming during immune activation promotes intracellular bacterial survival (glycerol or succinate)

| PRJNA578747 | ENA

Host metabolic reprogramming during immune activation promotes intracellular bacterial survival (2DG)

Project description:Intracellular pathogens, such as Salmonella enterica serovar Typhimurium (S.Tm), are able to sense and respond to a changing host cell environment. Macrophages exposed to microbial products undergo metabolic changes that are increasingly understood to drive a productive inflammatory response. However, the role of macrophage metabolic reprogramming in bacterial adaptation to the intracellular environment has not been explored. Here we show that changes in host metabolic state serve as a signal detected byS.Tm. Using metabolic profiling and dual RNA-seq, we show that succinate accumulates in infected macrophages and is sensed by intracellular S.Tm to promote induction of virulence genes. Succinate uptake by the bacterium drives induction of pmrAB-dependent genes and SPI-2 virulence-associated regulon. S.Tm lacking the DcuB transporter for succinate uptake display impaired intracellular survival. Our work demonstrates that accumulation of metabolic intermediates, necessary for macrophage activation, promote intracellular survival of pathogens, opening a new realm of metabolic host-pathogen crosstalk.

2022-10-19 | GSE139206 | GEO

The SON splicing factor is required for intracellular trafficking that promotes centriole assembly

Project description:The SON splicing factor is required for intracellular trafficking that promotes centriole assembly

| PRJNA689788 | ENA

Host metabolic reprogramming during immune activation promotes intracellular bacterial survival (host and bacteria)

2022-10-19 | GSE139205 | GEO

Host metabolic reprogramming during immune activation promotes intracellular bacterial survival (glycerol or succinate)

2022-10-19 | GSE139207 | GEO

Trained immunity suppression determines kidney allograft survival

Project description:Trained immunity suppression determines kidney allograft survival

| PRJNA1180533 | ENA

Trained immunity suppression determines kidney allograft survival

Project description:The innate immune system plays an essential role in regulating the immune responses to kidney transplantation, but the mechanisms through which innate immune cells influence long-term graft survival are unclear. The current study highlights the vital role of trained immunity in kidney allograft survival. Trained immunity describes the epigenetic and metabolic changes that innate immune cells undergo following an initial stimulus, allowing them have a stronger inflammatory response to subsequent stimuli. We stimulated healthy peripheral blood mononuclear cells with pretransplant and posttransplant serum of kidney transplant patients and immunosuppressive drugs in an in vitro trained immunity assay and measured tumor necrosis factor and interleukin 6 cytokine levels in the supernatant as a readout for trained immunity. We show that the serum of kidney transplant recipients collected 1 week after transplantation can suppress trained immunity. Importantly, we found that kidney transplant recipients whose serum most strongly suppressed trained immunity rarely experienced graft loss. This suppressive effect of posttransplant serum is likely mediated by previously unreported effects of immunosuppressive drugs. Our findings provide mechanistic insights into the role of innate immunity in kidney allograft survival, uncovering trained immunity as a potential therapeutic target for improving graft survival.

2024-11-04 | GSE280787 | GEO

Trained immunity suppression determines kidney allograft survival [ChIP]

Project description:Trained immunity suppression determines kidney allograft survival [ChIP]

| PRJNA1181014 | ENA