Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Human Airway Hyperresponsiveness

ABSTRACT: The purpose of this project is to gain a better understanding of the early cytokine-mediated mechanisms that lead to asthma. Keywords: time series, IL13

ORGANISM(S): Homo sapiens

PROVIDER: GSE3183 | GEO | 2005/08/24

SECONDARY ACCESSION(S): PRJNA92831

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Murine Airway Hyperresponsiveness

Project description:This project investigates the mechanisms that underlie asthma-related phenotypes associated with allergen exposure. See http://www.hopkins-genomics.org/asthma/asthma006/index.html The goal of the experiment was to identify genes that change their levels of expression as a consequence of challenge with allergen. The experiments utilized a murine model of human asthma that employed BALB/CJ mice. In this particular sensitization-challenge protocol, the response produced by BALB/CJ mice is representative of a majority of the mouse strains tested. The antigen complex used to sensitize and challenge the mice was ragweed pollen an allergen that is highly relevant to human disease. Keywords: time series, allergen

2005-08-24 | GSE3184 | GEO

Transcription profiling of human bronchial cell line treated with IL-13 to better understand early cytokine-mediated mechanisms that lead to asthma

Project description:The purpose of this project is to gain a better understanding of the early cytokine-mediated mechanisms that lead to asthma. Experiment Overall Design: 15 samples, 4 time points, 2 conditions. http://pepr.cnmcresearch.org/browse.do?action=list_prj_exp&projectId=95

2007-11-01 | E-GEOD-3183 | biostudies-arrayexpress

MicroRNA expression data from IL13-induced allergic airway inflammation of mice lungs

Project description:Epigenetic changes have been implicated in pathogenesis of asthma. We sought to determine if IL13, a key cytokine in airway inflammation and remodeling, induced miRNAs expression changes in the airways in conjunction with its transcriptional gene regulation. For our studies, we used a well-characterized transgenic mouse model of allergic airway inflammation induced by IL13. In this model, IL13 is conditionally overexpressed in the mouse lung when treated with doxycycline. Upon IL13 induction, these mice showed inflammatory cell infiltration, pronounced emphysema, increased pulmonary compliance, lung volume enlargement, mucus metaplasia, and increased expression of matrix metalloproteinases and cathepsins in the lung. The CC10-rtTA-IL13 transgenic (TG) and wildtype (WT) mice were treated with doxycycline for seven days. Mice were euthanized and the left upper lobes from all mice were removed for RNA extraction using the TRIzol method.

2012-02-23 | E-GEOD-35980 | biostudies-arrayexpress

MicroRNA expression data from IL13-induced allergic airway inflammation of mice lungs

2012-02-23 | GSE35980 | GEO

Methylated DNA immunoprecipitation (MeDIP) microarray data from IL13-induced allergic airway inflammation of mouse lungs

Project description:Epigenetic changes have been implicated in pathogenesis of asthma. We sought to determine if IL13, a key cytokine in airway inflammation and remodeling, induced epigenetic DNA methylation changes in the airways in conjunction with its transcriptional gene regulation. For our studies, we used a well-characterized transgenic mouse model of allergic airway inflammation induced by IL13. In this model, IL13 is conditionally overexpressed in the mouse lung when treated with doxycycline. Upon IL13 induction, these mice showed inflammatory cell infiltration, pronounced emphysema, increased pulmonary compliance, lung volume enlargement, mucus metaplasia, and increased expression of matrix metalloproteinases and cathepsins in the lung. We performed MeDIP microarray to examine the changes in DNA promoter methylation during IL13-induced allergic airway inflammation. The CC10-rtTA-IL13 transgenic (TG) and wildtype (WT) mice were treated with doxycycline for seven days. Mice were euthanized and the left lower lobes from all mice were removed for DNA extraction followed by MeDIP array analysis.

2012-04-06 | E-GEOD-37079 | biostudies-arrayexpress

Gene Expression Effects of IL-13 on Primary Human Airway Epithelial Cells

2012-12-04 | GSE37693 | GEO

Gene Expression Effects of IL-13 on Primary Human Airway Epithelial Cells

Project description:Primary culture airway epithelial cells, grown under physiologic air-liquid interface conditions, with, or without IL-13 in order to study the effects of this cytokine on mucous cell metaplasia, an important feature of asthma and COPD. Keywords: IL13, mucus, goblet cell RNA was isolated from primary culture airway epithelial cells grown at air-liquid interface, treated with or without IL-13 for 21 days.

2012-12-04 | E-GEOD-37693 | biostudies-arrayexpress

Methylated DNA immunoprecipitation (MeDIP) microarray data from IL13-induced allergic airway inflammation of mouse lungs

Project description:Epigenetic changes have been implicated in pathogenesis of asthma. We sought to determine if IL13, a key cytokine in airway inflammation and remodeling, induced epigenetic DNA methylation changes in the airways in conjunction with its transcriptional gene regulation. For our studies, we used a well-characterized transgenic mouse model of allergic airway inflammation induced by IL13. In this model, IL13 is conditionally overexpressed in the mouse lung when treated with doxycycline. Upon IL13 induction, these mice showed inflammatory cell infiltration, pronounced emphysema, increased pulmonary compliance, lung volume enlargement, mucus metaplasia, and increased expression of matrix metalloproteinases and cathepsins in the lung. We performed MeDIP microarray to examine the changes in DNA promoter methylation during IL13-induced allergic airway inflammation.

2012-04-07 | GSE37079 | GEO

Distinct Epithelial-Innate Immune Cell Transcriptional Circuits Underlie Airway Hyperresponsiveness in Asthma

Project description:Indirect airway hyperresponsiveness (AHR) is a highly specific feature of asthma but the underlying mechanisms responsible for driving indirect AHR remain incompletely understood. We aimed to identify differences in gene expression in epithelial brushings obtained from individuals with asthma who were characterized for indirect AHR in the form of exercise-induced bronchoconstriction (EIB). RNA-sequencing (RNA-seq) analysis was performed on epithelial brushings obtained from individuals with asthma with (n=11) and without EIB (n = 9).

2023-08-16 | GSE241016 | GEO

RGS4 controls airway hyperresponsiveness through GAP-independent mechanisms

Project description:Regulators of G protein signaling (RGS proteins) constrain G protein-coupled receptor (GPCR)-mediated and other responses throughout the body primarily, but not exclusively, through their GTPase activating (GAP) activity. Asthma is a highly prevalent condition characterized by airway hyper-responsiveness (AHR) to environmental stimuli resulting in part from amplified GPCR-mediated airway smooth muscle (ASM) contractility. Rgs2 or Rgs5 gene deletion in mice enhances AHR and ASM contraction whereas RGS4 knockout (KO) mice unexpectedly have decreased AHR due to increased production of the bronchodilator prostaglandin E2 (PGE2) by lung epithelial cells. Here we found that knockin mice harboring Rgs4 alleles encoding a point mutation (N128A) that sharply curtails RGS4 GAP activity had increased AHR, reduced airway PGE2 levels, and augmented GPCR-induced bronchial contraction compared to either RGS4 KO mice or WT controls. RGS4 interacted with the p85a subunit of PI3 kinase (PI3K) and inhibited PI3K-dependent PGE2 secretion elicited by TGFb in airway epithelial cells. Together these findings suggest that RGS4 affects asthma severity in part by regulating the airway inflammatory milieu in a G protein-independent manner.

2024-05-08 | GSE242546 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data