Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Tff1-expressing Tregs in lung prevents exacerbation of Bleomycin-induced pulmonary fibrosis (scRNA-Seq)

ABSTRACT: Bleomycin (BLM) induces lung injury, leading to inflammation and pulmonary fibrosis. Regulatory T cells (Tregs) maintain self-tolerance and control host immune responses. However, little is known about their involvement in the pathology of pulmonary fibrosis. Here we show that a unique Treg subset that expresses trefoil factor family 1(Tff1) emerges in the BLM-injured lung. These Tff1-expressing Tregs (Tff1-Tregs) were induced by IL-33. Moreover, although Tff1 ablation in Tregs had no impact, selective ablation of Tff1-Tregs using an intersectional genetic method promoted pro-inflammatory features of macrophages in the injured lung and exacerbated the fibrosis. Taken together, our study revealed the presence of a unique Treg subset expressing Tff1 in BLM-injured lungs and their critical role in the injured lung to ameliorate fibrosis.

ORGANISM(S): Mus musculus

PROVIDER: GSE267863 | GEO | 2024/08/19

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Tff1-expressing Tregs in lung prevents exacerbation of Bleomycin-induced pulmonary fibrosis (RNA-Seq)

Project description:Bleomycin (BLM) induces lung injury, leading to inflammation and pulmonary fibrosis. Regulatory T cells (Tregs) maintain self-tolerance and control host immune responses. However, little is known about their involvement in the pathology of pulmonary fibrosis. Here we show that a unique Treg subset that expresses trefoil factor family 1(Tff1) emerges in the BLM-injured lung. These Tff1-expressing Tregs (Tff1-Tregs) were induced by IL-33. Moreover, although Tff1 ablation in Tregs had no impact, selective ablation of Tff1-Tregs using an intersectional genetic method promoted pro-inflammatory features of macrophages in the injured lung and exacerbated the fibrosis. Taken together, our study revealed the presence of a unique Treg subset expressing Tff1 in BLM-injured lungs and their critical role in the injured lung to ameliorate fibrosis.

2024-08-19 | GSE267864 | GEO

Development and Preclinical Efficacy of Novel Transforming Growth Factor-β1 (TGFβ1) siRNAs for Pulmonary Fibrosis

Project description:Idiopathic pulmonary fibrosis is a chronic devastating disease of unknown etiology. No therapy is currently available. A growing body of evidence supports the role of TGFβ1 as the major player in the pathogenesis of the disease. This study designed novel human- and mouse-specific siRNAs and siRNA/DNA chimeras targeting both human and mouse common sequences and evaluated their inhibitory activity in pulmonary fibrosis induced by bleomycin and lung-specific transgenic expression of human TGFβ1. Selective novel sequences of siRNA and siRNA/DNA chimeras efficiently inhibited pulmonary fibrosis, indicating their applicability as tools for treating fibrotic disease in humans. Total RNA was extracted from lung tissue from mice with bleomycin (BLM)-induced lung fibrosis treated with mouse TGFβ1 siRNAs or vehicle on different days after BLM infusion.

2011-11-22 | E-GEOD-28122 | biostudies-arrayexpress

Tff1-expressing Tregs in lung prevents exacerbation of Bleomycin-induced pulmonary fibrosis (scRNA-Seq)

Project description:Tff1-expressing Tregs in lung prevents exacerbation of Bleomycin-induced pulmonary fibrosis (scRNA-Seq)

| PRJNA1113558 | ENA

Tff1-expressing Tregs in lung prevents exacerbation of Bleomycin-induced pulmonary fibrosis (RNA-Seq)

Project description:Tff1-expressing Tregs in lung prevents exacerbation of Bleomycin-induced pulmonary fibrosis (RNA-Seq)

| PRJNA1113556 | ENA

Ablation or Inhibition of Protein Disulfide Isomerase A3 (PDIA3) in Aberrant Club Cells Attenuates Osteopontin (SPP1) Production and Pulmonary Fibrosis

Project description:Rationale: The role of club cells in the pathology of Idiopathic Pulmonary Fibrosis IPF is not well understood. PDIA3, an endoplasmic reticulum (ER) based redox chaperone catalyzes the cysteine disulfide bonds (-S-S-) in various fibrosis-related proteins; however, mechanisms of action of PDIA3 in pulmonary fibrosis is not fully elucidated. Objectives: To examine the role of club cells and PDIA3 in the pathogenesis of pulmonary fibrosis (PF) and therapeutic potential of inhibition of PDIA3 in PF. Methods: The impact of PDIA3 and aberrant club cells in PF was studied by retrospective analysis of human transcriptome data from LGRC, and specific deletion and inhibition of PDIA3 in club cells and blocking Osteopontin (SPP1) downstream of PDIA3 in mice. Measurements and Main Results: The PDIA3 along with club cell secretory protein (SCGB1A1 or CCSP) signatures are upregulated in IPF compared to control patients, and PDIA3 increases correlate with a decrease in lung function in IPF patients. The Bleomycin (BLM) model of PF showed increases in aberrant CCSP and PDIA3 positive cells in the lung parenchyma. Ablation of Pdia3, specifically in CCSP cells, decreases CCSP cells along with PF in mice. The therapeutic administration of a PDI inhibitor LOC14 reversed the BLM-induced CCSP cells and PF in mice. The proteomic screen of the PDIA3 partners revealed SPP1 as a major interactor in PF. Blocking SPP1 attenuated the development of PF in mice. Conclusions: Collectively, this study demonstrates a new relationship of club cells, with PDIA3, SPP1, and a putative pathological function of club cells in pulmonary fibrosis.

2021-11-11 | PXD021715 | Pride

Disease modeling of pulmonary fibrosis using human iPS cell-derived alveolar organoids (fibroblasts)

Project description:We developed an in vitro model of pulmonary fibrosis using alveolar organoids, consisting of human induced pluripotent stem cell-derived alveolar epithelial cells and human lung fibroblasts. In this model, fibroblasts were activated by bleomysin (BLM) treatment in an epithelial cell-dependent manner simillar to the pathogenic mechanism of pulmonary fibrosis.

2021-11-19 | GSE172121 | GEO

An ageing bone marrow exacerbates lung fibrosis via a dysregulated regulatory T cell driven axis, fuelling profibrotic macrophage persistence

Project description:Pulmonary fibrosis is an incurable disease, which increasingly manifests with advanced age. Yet, how the ageing hematopoietic niche influences immune cell function and fibrosis progression in the lungs remains elusive. Using heterochronic transplant mouse models, we discovered that an aged bone marrow exacerbates lung fibrosis irrespective of lung tissue age. Upon lung injury, there was an increased pulmonary infiltration of monocyte-derived alveolar macrophages (Mo-AMs) from an aged bone marrow. These Mo-AMs displayed an enhanced profibrotic profile and a delayed transition in acquiring a homeostatic tissue-resident phenotype. This impaired Mo-AM differentiation was attributed to diminished numbers of regulatory T cells (Tregs) and the reduced availability of the anti-inflammatory cytokine IL-10 in the lung microenvironment of mice engrafted with aged bone marrow. Mechanistically, we show that Tregs are crucial providers of IL-10 that promote timely Mo-AM maturation and attenuate fibrosis progression. Our findings demonstrate the critical influence of an aged bone marrow on the development of lung fibrosis and identify a Treg-mediated resolutory axis as a potential therapeutic target for accelerated tissue repair.

2024-12-16 | GSE277799 | GEO

An ageing bone marrow exacerbates lung fibrosis via a dysregulated regulatory T cell driven axis, fuelling profibrotic macrophage persistence.

2024-12-02 | GSE274253 | GEO

Disease modeling of pulmonary fibrosis using human iPS cell-derived alveolar organoids (SPC+ cells)

2021-11-19 | GSE172122 | GEO

Gene expression data from bleomycin-instilled lung tissue or control (Sham) of C57BL/6 mice (wild-type mice and transgenic mice expressing dominant-negative form of p38α or constitutive active form of MKK6 in type II alveolar epithelial cells).

Project description:Idiopathic pulmonary fibrosis (IPF) is a type of pulmonary fibrosis, a disease that results in scarring and stiffness of lung tissue affecting over 5 million people globally, while the underlying disease mechanisms in IPF are largely unknown. As an animal model of IPF, a single intratracheal injection of bleomycin (BLM) is generally employed, in which cell death of type II alveolar epithelial cells (AEC II) is a trigger of pulmonary fibrosis. One of mitogen-activated protein kinases, p38 is well known as an important regulator of inflammatory responses and cell fate such as apoptosis, differentiation and tumorgenesis. Given that mice with different intrinsic activity of p38 in AEC II were subjected to BLM instillation and investigated, candidate genes in the development of pulmonary fibrosis would be screened. Here, we provide gene expression profiling of lung tissues using the RNA sequencing for identifying changes in gene expression.

2020-09-09 | GSE154074 | 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