Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Serum Amyloid A proteins reduce bone mass during mycobacterial infections

ABSTRACT: To investigate the molecular mechanisms responsible for bone loss during mycobacterial infections

ORGANISM(S): Mus musculus

PROVIDER: GSE215856 | GEO | 2023/05/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Genetic Basis of Pulmonary Non-tuberculous Mycobacterial Infections

Project description:<p>This project aims at characterizing the human host susceptibility to pulmonary non-tuberculous mycobacterial (PNTM) infections. PNTM infections occur in patients with chronic lung disease, but also in a distinct group of elderly women without lung defects but who share a common body morphology: tall and lean with scoliosis, pectus excavatum, and mitral valve prolapse. We performed whole exome and genome sequencing in extended families of patients with active PNTM. This unique collection of familial cohorts in PNTM represents an important opportunity for a high yield search for genes that regulate mucosal immunity. We also sequenced the genome of mycobacterial isolates from PNTM patients to integrate host PNTM susceptibility with mycobacterial genotypes and gain insights into the key factors involved in this devastating disease.</p>

| phs000719 | dbGaP

Patients affected with autosomal dominant monocytopenia with increased susceptibility to mycobacterial infection

Project description:We identified 18 patients with the distinct clinical phenotype of disseminated nontuberculous mycobacterial infections, viral infections, especially with human papillomaviruses, and fungal infections, primarily histoplasmosis and molds. This syndrome typically had its onset in adulthood and was characterized by profound circulating monocytopenia, B lymphocytopenia, and NK lymphocytopenia. T lymphocytes were variably affected. Despite these peripheral cytopenias, all patients had macrophages and plasma cells at sites of inflammation and normal immunoglobulin levels. This novel clinical syndrome links mycobacterial, viral, and fungal susceptibility with malignancy and is transmitted in an autosomal dominant pattern. In order to elucidate the possible genetic defect that results in this novel clinical syndrome, we performed microarray expression analysis on polymorphonuclear leukocytes (PMNs) isolated from affected patients and healthy controls. Keywords: healthy donor vs affected patient

2010-01-01 | GSE16020 | GEO

Diversity of nontuberculous mycobacterial infections in Kuwait: rapid identification and differentiation of Mycobacterium species by multiplex PCR, INNO-LiPA Mycobacteria v2 assay and PCR-sequencing of rDNA

Project description:Diversity of nontuberculous mycobacterial infections in Kuwait

| PRJEB29664 | ENA

Transcription profiling of polymorphonuclear leukocyte from patients affected with autosomal dominant monocytopenia and an increased susceptibility to mycobacterial infection.

2010-01-01 | E-GEOD-16020 | biostudies-arrayexpress

Mycobacterial communities in pulmonary NTM

Project description:Profiling Mycobacterial Communities in Pulmonary Nontuberculous Mycobacterial Disease

| PRJEB22153 | ENA

Human hookworm infection enhances mycobacterial growth inhibition and associates with reduced risk of tuberculosis infection.

Project description:Soil-transmitted helminths and Mycobacterium tuberculosis frequently coincide geographically and it is hypothesized that gastrointestinal helminth infection may exacerbate tuberculosis (TB) disease by suppression of Th1 and Th17 responses. However, few studies have focused on latent TB (LTBI) infection, which predominates globally. We performed a large observational study of healthy adults migrating from Nepal to the UK (n=645). Individuals were screened for LTBI and gastrointestinal parasite (GIP) infections. A significant negative association between hookworm (HW) and LTBI-positivity was seen (OR=0.221; p=0.039). HW treatment did not effect LTBI conversions. Blood from individuals with HW had a significantly greater ability to control virulent mycobacterial growth in vitro than from those without, which was lost following HW treatment. There was a significant negative relationship between mycobacterial growth and eosinophil counts. We also analysed differential gene expression among individuals with and without HW infection, pre- and post- anti-helminth treatment. Eosinophil-associated differential gene expression characterised the whole blood transcriptome of hookworm infection and correlated with improved mycobacterial control. These data provide a potential alternative explanation for the reduced prevalence of LTBI among individuals with HW infection, and possibly an anti-mycobacterial role for helminth-induced eosinophils.

2018-12-26 | GSE122737 | GEO

Sensing of mycobacterial arabinogalactan by galectin-9 exacerbates mycobacterial infection by inducing matrix metalloproteinases

Project description:Mycobacterial arabinogalactan (AG) is an essential cell wall component of Mycobacteria and a frequent structural and bio-synthetical target for anti-tuberculosis (TB) drug development. Yet, it is unclear whether mycobacterial AG is a pathogen-associated molecular pattern (PAMP) with an elusive pattern recognition receptor (PRR). Here, we report that mycobacterial AG is recognized by galectin-9 and exacerbates mycobacterial infection. Administration of AG-specific aptamers inhibited cellular infiltration caused by Mycobacterium tuberculosis (Mtb) or Mycobacterium bovis BCG, and moderately increased survival of Mtb-infected mice or Mycobacterium marinum-infected zebrafish. AG interacted with carbohydrate recognition domain (CRD) 2 of galectin-9 with high affinity, and galectin-9 associated with transforming growth factor β-activated kinase 1 (TAK1) via CRD2 to trigger subsequent activation of extracellular signal-regulated kinase (ERK) as well as induction of the expression of matrix metalloproteinases (MMPs). Moreover, deletion of galectin-9 or inhibition of MMPs blocked AG-induced pathological impairments in the lung, and the AG-galectin-9 axis aggravated the process of Mtb infection in mice. These results demonstrate that AG is an important virulence factor of mycobacteria and galectin-9 is a novel receptor for Mtb and other mycobacteria, paving the way for the development of novel effective TB immune modulators.

2021-02-17 | GSE166850 | GEO

Mycobacterial TDM Reprograms Macrophage Global Gene Expression

Project description:Effect of mycobacterial cell wall component TDM (trehalose dimycolate) of murine macrophage gene expression.

2013-03-09 | E-MEXP-3814 | biostudies-arrayexpress

Expression analysis for detection of mycobacterial transcripts present in exosomes derived from M.tb infected macrophages

Project description:Mycobacterial transcripts were identified in exosomes released from M.tb infected RAW264.7 macrophages that were not present in uninfected exosomes suggesting export of mycobacterial RNA via exosomes Mycobacterial RNA was used as positive control and RNA from exosomes released from uninfected macrophages was used as negative control

2014-09-15 | GSE54444 | GEO

Effect of Mycobacterial EST12 on gene expression of RAW264.7 cells

Project description:Mouse RAW264.7 cells were stimulated with 2 uM purfied recombinant Mycobacterial EST12 protein for 0 h or 3 h

2022-08-05 | GSE210089 | GEO