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

Similar Datasets

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 (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

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

2022-10-19 | GSE139207 | GEO

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

2022-10-19 | GSE139205 | GEO

RIG-I is an intracellular checkpoint that limits CD8+ T-cell antitumor immunity

Project description:RIG-I is a pattern recognition receptor involved in innate immunity, but its role in adaptive immunity remains unclear. Here, we demonstrate that RIG-I is upregulated in tumor infiltrating CD8+ T cells, where it functions as an intracellular checkpoint to negatively regulate CD8+ T cell function and limit antitumor immunity. Mechanically, up-regulation of RIG-I in CD8+ T cells is induced by retinoic acid (RA), a metabolite of vitamin A in TME, and direct inhibits the AKT/glycolysis signaling pathway. In addition, deletion of RIG-I enhances the efficacy of adoptively transferred T cells against solid tumors and inhibition of RIG-I enhances the response to PD-1 blockade. Our findings identify RIG-I as an intracellular checkpoint and a potential target for alleviating inhibitory constraints on T cells in cancer immunotherapy, either alone or in combination with immune checkpoint blockade.

2023-04-25 | GSE230045 | GEO

A late blight effector promotes a plant growth and development pathway to antagonise immunity

Project description:To effectively manage resources, regulatory cross-talk between biological processes within an organism is essential. An emerging area in plant research focuses on antagonism between regulatory systems controlling growth/development and those governing immunity. Such crosstalk represents a point of vulnerability for pathogens to exploit. Here we show that the notorious potato blight pathogen Phytophthora infestans promotes a growth and development pathway in order to antagonise plant immunity. AVR2, an effector protein secreted by P. infestans, has been shown to interact with potato BSL1, a putative phosphatase implicated in brassinosteroid hormone signalling. Plants expressing AVR2 exhibit transcriptional and phenotypic overlaps with an over-active brassinosteroid signalling pathway, and have compromised immunity. The activity of AVR2 leads to up-regulation of a functional orthologue of AtHBI1, known to facilitate cross-talk between the brassinosteroid pathway and immune signalling in Arabidopsis. Transient expression of potato HBI1-like compromises immunity and enhances leaf colonisation by P. infestans. Knowledge of how pathogens manipulate regulatory cross-talk governing resource allocation in plants will inform crop breeding efforts of the future; helping to maximise both yield and resistance to ensure food security as pressure on our agricultural systems increases.

2017-03-01 | E-MTAB-3854 | biostudies-arrayexpress

Immunity to commensal skin fungi promotes psoriasiform skin inflammation

Project description:Immunity to commensal skin fungi promotes psoriasiform skin inflammation

| PRJNA605153 | ENA

Human variation impacting MCOLN2 restricts Salmonella Typhi replication by magnesium deprivation

Project description:Human genetic diversity can reveal critical factors in host-pathogen interactions. This is especially useful for human-restricted pathogens like Salmonella enterica serovar Typhi (S. Typhi), the cause of Typhoid fever. One key dynamic during infection is competition for nutrients: host cells attempt to restrict intracellular replication by depriving bacteria of key nutrients or delivering toxic metabolites in a process called nutritional immunity. Here, a cellular genome-wide association study of intracellular replication by S. Typhi in nearly a thousand cell lines from around the world—and extensive follow-up using intracellular S. Typhi transcriptomics and manipulation of magnesium concentrations—demonstrates that the divalent cation channel mucolipin-2 (MCOLN2) restricts S. Typhi intracellular replication through magnesium deprivation. Our results reveal natural diversity in Mg2+ limitation as a key component of nutritional immunity against S. Typhi.

2023-01-05 | GSE222194 | GEO

SEC23B-dependent COPII Vesicles Regulate T Cell Immunity

Project description:The coordinated release of proteins by T cells enables controlled biological responses. While the molecular mechanisms underlying T cell secretion are being increasingly understood, whether the critical ER-to-Golgi trafficking pathway regulates T cell immunity is not known. We utilized mice with a T cell-specific deletion of SEC23B, a core subunit of Coat Protein Complex II (COPII) which drives ER-to-Golgi cargo transport. We found that following activation, SEC23B-deficient T cells display an altered secretome compared to wild-type, which includes reduced secretion of T cell-derived inflammatory mediators, and which is associated with functional ramifications in vitro and in vivo. Together, these data reveal a critical role for the SEC23B-dependent COPII pathway in T cell immunity.

2021-09-08 | PXD015766 | Pride

A glycolytic enzyme enoalse negatively regulates plant immunity by repressing intracellular immune receptor NLR genes

Project description:A glycolytic enzyme enoalse negatively regulates plant immunity by repressing intracellular immune receptor NLR genes

| PRJNA657243 | ENA