Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Inhibition of granuloma triglyceride synthesis imparts control of Mycobacterium tuberculosis through curtailed inflammatory responses

ABSTRACT: We report the impact of granuloma triglyceride lowering on progression of infection in the C3HeB/FeJ mouse model.

ORGANISM(S): Mus musculus

PROVIDER: GSE179437 | GEO | 2021/09/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Inhibition of granuloma triglyceride synthesis imparts control of Mycobacterium tuberculosis through curtailed inflammatory responses

Project description:Inhibition of granuloma triglyceride synthesis imparts control of Mycobacterium tuberculosis through curtailed inflammatory responses

| PRJNA743689 | ENA

In-vivo Gene Signatures of Mycobacterium tuberculosis In C3HeB/FeJ Mice

Project description:In-vivo Gene Signatures of Mycobacterium tuberculosis In C3HeB/FeJ Mice In this experiment we have compared Mtb transcriptomics in-vivo, using samples derived from chronically infected C3HeB/FeJ mice, which produce human like caseating lesions, unlike other murine species, to Mtb cultured in-vitro. Similarly, the genome-wide expression of MtbdeldosR, MtbdeldosS and MtbdeldosT mutants is also compared between lungs from C3HeB/FeJ mice and in-vitro culturing.

2015-07-11 | E-GEOD-70765 | biostudies-arrayexpress

In-vivo Gene Signatures of Mycobacterium tuberculosis In C3HeB/FeJ Mice

Project description:In-vivo Gene Signatures of Mycobacterium tuberculosis In C3HeB/FeJ Mice

2015-07-11 | GSE70765 | GEO

Inhibition of Granuloma Triglyceride Synthesis Imparts Control of <i>Mycobacterium tuberculosis</i> Through Curtailed Inflammatory Responses.

Project description: Not available

| S-EPMC8479166 | biostudies-literature

Genome-wide characterization of a novel necrotic granuloma model of latent tuberculosis infection and reactivation in mice

Project description:We sought to develop and characterize a novel paucibacillary model in mice, which develop necrotic lung granulomas following infection with Mycobacterium tuberculosis. Paucibacillary infection was established, recapitulating the sterilizing activities of human LTBI regimens. TNF neutralization led to increased lung bacillary load, disrupted granuloma architecture with expanded necrotic foci and reduced tissue hypoxia, and accelerated animal mortality. TNF-neutralized mouse lungs and sera showed significant upregulation of IFN?, IL-1?, IL-6, IL-10, CCL2, CCL3, and matrix metalloproteinase genes Six weeks after aerosol-immunization with recombinant M. bovis BCG overexpressing the 30-kilodalton antigen, C3HeB/FeJ mice were aerosol-infected with M. tuberculosis H37Rv. Six weeks later, mice were treated with one of three standard regimens for latent TB infection (LTBI) or TNF-neutralizing antibody. Mouse lungs were analyzed by histology, positron emission tomography/computed tomography, whole-genome microarrays, and RT-PCR. Lungs and sera were studied by multiplex enzyme-linked immunosorbent assays

2014-02-20 | E-GEOD-55183 | biostudies-arrayexpress

Comparison of liver and kidney from wildtype C3HeB/FeJ mice

Project description:Comparison of kidney and liver samples from wildtype C3HeB/FeJ mice. 16 dual-color DNA-chip hybridizations of cDNAs from three age-matched male mice were made. For each individual mouse 6 or 4 replicate hybridizations were done. Keywords = liver Keywords = kidney Keywords = C3HeB/FeJ Keywords: other

2004-10-15 | GSE1696 | GEO

Mycobacterium tuberculosis H37Rv

Project description:In-vivo Gene Signatures of Mycobacterium tuberculosis In C3HeB/FeJ Mice

| PRJNA289506 | ENA

Single cell analysis of Granuloma crypt epithelium

Project description:The purpose of this study is to compare the cellular populations present within granuloma (Sca1+) and non-granuloma (Sca-1–) crypt epithelum arising from parasitic H polygyrus infections.

2018-04-12 | GSE108233 | GEO

Macrophage Epithelial Reprogramming Underlies Mycobacterial Granuloma Formation and Promotes Infection

Project description:Mycobacterium tuberculosis infection in humans triggers formation of granulomas, tightly organized immune cell aggregates that are the central structure of tuberculosis. Infected and uninfected macrophages interdigitate, assuming an altered, flattened appearance. Although pathologists have described these changes for over a century, the molecular and cellular programs underlying this transition are unclear. We find that mycobacterial granuloma formation is accompanied by macrophage induction of canonical epithelial molecules and structures. Using the zebrafish-Mycobacterium marinum model, we identify fundamental macrophage reprogramming events that parallel E-cadherin-dependent mesenchymal-epithelial transitions. Macrophage-specific disruption of E-cadherin function results in disordered granuloma formation, enhanced immune cell access, decreased bacterial burden and increased host survival, suggesting that the granuloma can also serve a bacteria-protective role. In humans, we find that granuloma macrophages are similarly transformed. Long considered largely through the prism of immune signaling pathways, granuloma macrophages are reprogrammed by epithelial modules that alter the trajectory of mycobacterial infection.

2016-10-18 | GSE81913 | GEO

Mus musculus strain:C3HeB/FeJ

Project description:Mus musculus strain:C3HeB/FeJ Transcriptome or Gene expression

| PRJNA396045 | ENA