Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Global transcriptomic investigation of the human macrophage response towards pathogenic/non-pathogenic mycobacteria

ABSTRACT: Global transcriptomic investigation of the human macrophage response towards pathogenic/non-pathogenic mycobacteria

PROVIDER: PRJNA505785 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Global transcriptomic investigation of the human macrophage response towards pathogenic/non-pathogenic mycobacteria

Project description:We present an infection study with pathogenic and non-pathogenic mycobacterial strains that have vastly different characteristics. The early/late host response to infection with these detergent-free cultured strains will be analysed through Ampliseq and further validated through qPCR in an attempt to provide information on the subtleties which may ultimately contribute to the virulent phenotype. Proceeding to the next objective of the study is to knock-down (siRNA)/knock-up (saRNA) selected differentially expressed mRNA to study their role in the intracellular survival of M. tuberculosis

2019-12-02 | GSE122619 | GEO

A conserved aminopeptidase PepN, exhibits divergent traits in pathogenic and non- pathogenic mycobacteria

Project description:A conserved aminopeptidase PepN, exhibits divergent traits in pathogenic and non- pathogenic mycobacteria

2019-11-12 | PXD008790 | Pride

IRF5 promotes intestinal inflammation by guiding monocyte differentiation towards pathogenic CD11c+ macrophage phenotype

Project description:IRF5 promotes intestinal inflammation by guiding monocyte differentiation towards pathogenic CD11c+ macrophage phenotype

| PRJNA530678 | ENA

IRF5 promotes intestinal inflammation by guiding monocyte differentiation towards pathogenic CD11c+ macrophage phenotype [scrnaseq_steady_state]

Project description:IRF5 promotes intestinal inflammation by guiding monocyte differentiation towards pathogenic CD11c+ macrophage phenotype [scrnaseq_steady_state]

| PRJNA638619 | ENA

IRF5 promotes intestinal inflammation by guiding monocyte differentiation towards pathogenic CD11c+ macrophage phenotype [small_bulk_rnaseq]

Project description:IRF5 promotes intestinal inflammation by guiding monocyte differentiation towards pathogenic CD11c+ macrophage phenotype [small_bulk_rnaseq]

| PRJNA530686 | ENA

IRF5 promotes intestinal inflammation by guiding monocyte differentiation towards pathogenic CD11c+ macrophage phenotype [single_cell_rnaseq]

Project description:IRF5 promotes intestinal inflammation by guiding monocyte differentiation towards pathogenic CD11c+ macrophage phenotype [single_cell_rnaseq]

| PRJNA530685 | ENA

Mildly pathogenic Rickettsia-macrophage interactions

Project description:The molecular details underlying differences in pathogenicity between Rickettsia species remain to be fully understood. Evidence points to macrophage permissiveness as a key mechanism in rickettsial virulence. Different studies have shown that several rickettsial species responsible for mild forms of rickettsioses can also escape macrophage-mediated killing mechanisms and establish a replicative niche within these cells. However, their manipulative capacity with respect to host cellular processes is far from being understood. A deeper understanding of the interplay between mildly pathogenic rickettsiae and macrophages and the commonalities and specificities of host responses to infection would illuminate differences in immune evasion mechanisms and pathogenicity. We have used quantitative proteomics by SWATH-MS/MS to profile alterations resulting from infection of THP-1 macrophages with three mildly pathogenic rickettsiae: R. parkeri, R. africae, and R. massiliae, all successfully proliferating in these cells. We show that all three species trigger different proteome signatures. Our results reveal a significant impact of infection in proteins categorized as type-I interferon responses, here included several components of the RIG-1-like signaling pathway, mRNA splicing, and protein translation. Moreover, significant differences in protein content between infection conditions anticipate species-specific induced alterations. Indeed, we confirm a distinct impact on host inflammatory responses between species during infection, demonstrating that these species trigger different levels of INF-β, differences in the bioavailability of the pro-inflammatory cytokine IL1-β, and in triggering pyroptotic events. This work reveals novel aspects and exciting nuances of macrophage-Rickettsia interactions, adding additional layers of complexity between Rickettsia and host cells constant arms race for survival.

2022-01-11 | PXD026982 | Pride

IRF5 promotes intestinal inflammation by guiding monocyte differentiation towards pathogenic CD11c+ macrophage phenotype [scrnaseq_steady_state]

Project description:Mononuclear phagocytes (MNPs) play a key role in maintaining intestinal homeostasis but also in triggering immunopathology in response to acute microbial stimulation, which induces the recruitment of masses of Ly6Chi monocytes to the gut. The regulators that control monocyte tissue adaptation in the gut remain poorly understood. Interferon Regulatory Factor 5 (IRF5) is a transcription factor previously shown to play a key role in maintaining the inflammatory phenotype of macrophages Here we investigate the impact of IRF5 on the MNP system and physiology of the gut at homeostasis and during inflammation. We demonstrate that IRF5 deficiency has a limited impact on colon physiology at steady state, but ameliorates immunopathology during Helicobacter hepaticus induced colitis. Inhibition of IRF5 activity in MNPs phenocopies global IRF5 deficiency. Using a combination of bone marrow chimera and single cell RNA-sequencing approaches we compare the differentiation trajectories of wild type and IRF5 deficient monocytes in a shared inflammatory environment and demonstrate that IRF5 stipulates a choice in monocyte differentiation towards macrophages. Specifically, IRF5 promotes the generation of pathogenic CD11c+ macrophages and controls the production of inflammatory mediators by these cells. Thus, we identify IRF5 as a key transcriptional controller of pathogenic monocyte differentiation in the gut.

2020-06-11 | GSE152198 | GEO

IRF5 promotes intestinal inflammation by guiding monocyte differentiation towards pathogenic CD11c+ macrophage phenotype [small_bulk_rnaseq]

2020-04-01 | GSE129257 | GEO

IRF5 promotes intestinal inflammation by guiding monocyte differentiation towards pathogenic CD11c+ macrophage phenotype [single_cell_rnaseq]

2020-04-01 | GSE129256 | GEO