Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

An IL-9-pulmonary macrophage axis defines the allergic lung inflammatory environment

ABSTRACT: An IL-9-pulmonary macrophage axis defines the allergic lung inflammatory environment

PROVIDER: PRJNA683661 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

An IL-9-pulmonary macrophage axis defines the allergic lung inflammatory environment

Project description:Despite IL-9 functioning as a pleiotropic cytokine in mucosal environments, the IL-9 responsive cell repertoire is still not well defined. Here, we found IL-9 mediates pro-allergic activities by targeting lung macrophages. IL-9 inhibits alveolar macrophage expansion and promotes recruitment of monocytes that develop into CD11c+/- interstitial macrophage populations. Interstitial macrophages were required for IL-9-dependent allergic responses. Mechanistically, IL-9 affects the function of lung macrophages by inducing Arg1 activity. Compared to Arg1-deficient lung macrophages, Arg1-expressing macrophages co-express greater amounts of CCL5. Adoptive transfer of Arg1+ lung macrophages but not Arg1- lung macrophages can recover allergic inflammation that is lost in Il9r-/- mice. In parallel, the elevated expression of IL-9, IL-9R, Arg1 and CCL5 is correlated with disease in asthma patients. Thus, our study uncovers an IL-9/macrophage/Arg1 axis as a potential therapeutic target for allergic airway inflammation.

2021-11-15 | GSE162898 | GEO

The USP7-STAT3-granzyme-Par-1 axis regulates allergic inflammation by promoting differentiation of IL-5-producing Th2 cells

Project description:Uncontrolled type 2 immunity by type 2 helper T (Th2) cells causes intractable allergic diseases; however, whether the interaction of CD4+ T cells shapes the pathophysiology of allergic diseases remains unclear. We identified a subset of Th2 cells that produced the serine proteases granzyme A and B early in differentiation. Granzymes cleave protease-activated receptor (Par)-1 and induce phosphorylation of p38 mitogen-activated protein kinase (MAPK), resulting in the enhanced production of IL-5 and IL-13 in both mouse and human Th2 cells. Ubiquitin-specific protease 7 (USP7) regulates IL-4-induced phosphorylation of STAT3, resulting in granzyme production during Th2 cell differentiation. Genetic deletion of Usp7 or Gzma and pharmacological blockade of granzyme B ameliorated allergic airway inflammation. Furthermore, PAR-1+ and granzyme+ Th2 cells were colocalized in nasal polyps from patients with eosinophilic chronic rhinosinusitis. Thus, the USP7-STAT3-granzymes-Par-1 pathway is a potential therapeutic target for intractable allergic diseases.

2023-11-13 | GSE229875 | GEO

Altered response of macrophages to an inflammatory stimulus in an allergic environment

Project description:To investigate how an allergic cytokine environment (associated with increased levels of IL4 and IL-13) alters the response of macrophages to a pro-inflammatory stimulus.

2018-02-12 | GSE109372 | GEO

Axis axis

Project description:Axis axis overview

| PRJNA194246 | ENA

IL-33/IL-31 Axis in Immune-Mediated and Allergic Diseases.

Project description: Not available

| S-EPMC6929191 | biostudies-literature

SLAM-seq defines direct gene-regulatory functions of the BRD4-MYC axis

Project description:SLAM-seq defines direct gene-regulatory functions of the BRD4-MYC axis

| PRJNA437109 | ENA

TLR9-IL-2 axis exacerbates allergic asthma by preventing IL-17A hyperproduction.

Project description: Not available

| S-EPMC7581806 | biostudies-literature

IL-22 inhibits allergic airway inflammation in house dust mite-induced asthma models

Project description:While the pathogenesis of asthma is mainly orchestrated by antigen-specific Th2 cells and their cytokines, recent findings indicate the involvement of other subsets of helper T cells including Th17 cells. Previous studies have shown that IL-22, one of Th17 cell-related cytokines, plays multiple roles in regulating allergic airway inflammation; however, the mechanism underlying the Il-22-mediated regulation remains unclear. Here, we show that allergic airway inflammation upon intratracheal administration of house dust mite extract (HDM), a representative allergen, were exacerbated in IL-22-deficient mice. To address the molecular mechanisms by which IL-22 inhibits the development of HDM-induced allergic airway inflammation, we next performed an unbiased comprehensive screening of genes induced by IL-22 administration in the lung by RNA-seq analysis.

2017-08-10 | GSE100858 | GEO

Targeting mitochondrial reactive oxygen species alleviates allergic airway disease in a mouse model of obese allergic asthma

Project description:Obesity is associated with severe, difficult to control asthma, and increased airway oxidative stress. Mitochondrial reactive oxygen species (mROS) are an important source of oxidative stress leading us to hypothesize that targeting mROS in obese allergic asthma might be an effective treatment strategy. Using a mouse model of house dust mite (HDM) induced allergic airway disease in mice fed a low- (LFD) or high-fat diet (HFD), and the mitochondrial antioxidant MitoQuinone (MitoQ); we investigated the effects of obesity and mROS on airway inflammation, remodelling and airway hyperreactivity (AHR). HDM induces airway inflammation, remodelling and hyperreactivity in both lean and obese mice. Obese allergic mice showed increased lung tissue eotaxin levels, airway tissue eosinophilia and AHR when compared to lean allergic mice. MitoQ reduced markers of airway inflammation, remodelling and hyperreactivity in both lean and obese allergic mice, and tissue eosinophilia in obeseHDM mice. mROS regulates cell signalling by protein oxidation of multiple downstream targets: MitoQ reduced HDM-induced cysteine-sulfenylation of several proteins including those involved in the unfolded protein response (UPR). In summary, mROS mediates the development of allergic airway disease and hence MitoQ might be effective for the treatment for asthma, and specific features of obese asthma.

2023-06-02 | PXD029715 | Pride

Murine lung transcripts during soluble egg antigen (SEA)-induced allergic asthma and bleomycin-induced pulmonary fibrosis in Wildtype, IL-13Ra1 and IL-13Ra2 deficient mice sensitized and challenged

Project description:Transcriptional profiling of mouse lungs by comparing PBS and saline treated lungs with SEA and bleomycin treated lungs, respectively. Mice strains used in this study include wild type (C57BL/6), IL-13Ra1 and IL-13Ra2 deficient mice. In mouse model of allergic asthma, mice were sensitized twice (day0 and day14) by i.p. injection of 10 µg of SEA. On days 28 and 31 mice were anesthetized with a mixture of xylazine and ketamine and given an intratracheal (I.T) airway challenge with 10 µg of SEA. Mice were sacrificed 24 h after the final airway challenge (day 32) and lungs were collected for RNA preparation. Biological replicates include 5 PBS treated and 5 SEA treated mice. In bleomycin-induced fibrosis odel, mice were anaesthetized with a xylazine and ketamine cocktail and given 0.15 U bleomycin sulfate (EMD) in saline or saline alone via the I.T. route. On day 7, mice were sacrificed and ungs were collected for RNA preparation. Biological replicates include 4 saline treated and 4 bleomycin treated mice. Goal was to determine IL-13 receptors regulated genes during SEA induced allergic asthma and bleomycin-induced fibrosis. Fluorescent cDNA targets were prepared from a 20 μg experimental RNA sample (SEA or bleomycin challenged group–dUTPCy5 – Amersham, Piscataway, NJ) and a 20 μg reference RNA sample (PBS or saline treated group–dUTPCy3- Amersham, Piscataway, NJ). Equal quantities of the above labeled cDNA (experimental and reference labeled RNA samples) were mixed and any free label present in the sample was removed by washing 3 times using a 10 kDa cutoff Vivaspin filters (Millipore). Labeled fluorescent cDNA targets were hybridized on the Whole Mouse Genome Oligo Microarray Kit (Agilent, Palo Alto, CA) containing more than 41000 gene probes.

2011-09-06 | E-GEOD-27721 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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