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Resolution of Cystic Fibrosis Lung Disease and Inflammation Driven by Mucus Obstruction with Resolvin D1

ABSTRACT: Resolution of Cystic Fibrosis Lung Disease and Inflammation Driven by Mucus Obstruction with Resolvin D1

PROVIDER: PRJNA983324 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24910876_1.fastq.gz	Fastqsanger.gz
	SRR24910877_1.fastq.gz	Fastqsanger.gz
	SRR24910878_1.fastq.gz	Fastqsanger.gz
	SRR24910879_1.fastq.gz	Fastqsanger.gz
	SRR24910880_1.fastq.gz	Fastqsanger.gz

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Resolution of Cystic Fibrosis Lung Disease and Inflammation Driven by Mucus Obstruction with Resolvin D1

Project description:Progressive lung disease remains the major cause of morbidity and mortality of people with cystic fibrosis (CF). CF lung disease evolves from mucus obstruction into non-resolving airway inflammation, bronchiectasis, and damage that impairs respiratory and fitness activity. Therefore, therapeutic strategies that promote resolution of airway inflammation in CF to alleviate the burden of airflow obstruction and improve physical capacity are of wide interest. Here, we report that the proresolving lipid mediator resolvin (Rv) D1 halts mucus-driven inflammation in CF human cells and in vivo. RvD1 dampened migration and pathogenic phenotypes of neutrophils from volunteers with CF as well as inflammatory signaling pathways of CF bronchial epithelial cells triggered by CF mucus. In mice overexpressing the β-subunit of the epithelial Na+ channel (βENaC) RvD1 administration prevented and reverted lung inflammation caused by mucus accumulation and promoted the resolution of pulmonary exacerbation caused by P. aeruginosa. RvD1 also significantly improved physical activity and energy expenditure that are impaired in βENaC mice compared to wild type littermates. These findings demonstrate efficacy of RvD1 in enhancing resolution of lung disease and chronic inflammation associated with mucus obstruction and provide proof of concept for its potential therapeutic approach in FC.

2023-10-10 | GSE234839 | GEO

Resolvin D1 improves allograft osteointegration and directly enhances osteoblasts differentiation

Project description:Resolvin D1 improves allograft osteointegration and directly enhances osteoblasts differentiation

2023-02-08 | GSE224195 | GEO

Gene expression profile at single cell level of leukocytes from transplanted syngeneic left lung grafts following treatment with Resolvin D1.

Project description:Neutrophils play a pivotal role in the pathogenesis of lung ischemia-reperfusion injury. The effect of pro-resolving lipid mediators, such as Resolvin D1, on early neutrophil trafficking has not been assessed in organ transplantation. We obtained single-cell RNA sequencing of leukocytes from syngeneic left lung grafts to elucidate the genetic changes induced by recipient treatment with Resolvin D1 or vehicle.

2023-07-15 | GSE237110 | GEO

Resolvin D1 improves allograft osteointegration and directly enhances osteoblasts differentiation

Project description:Resolvin D1 improves allograft osteointegration and directly enhances osteoblasts differentiation

| PRJNA930040 | ENA

p38 Mitogen-Activated Protein Kinase Signals the Immunoresolving Actions of Resolvin D1 in Inflamed Human Visceral Adipose Tissue

Project description:Activation of the innate immune system leading to a persistent state of low-grade of tissue inflammation greatly influences the risk of developing metabolic complications associated with obesity. In this study, we characterized the inflammatory state in adipose tissue from obese patients and explored the potential of the specialized pro-resolving mediator (SPM) resolvin D1 (RvD1) to actively terminate inflammation and promote its resolution. By means of high-troughput transcritomic analysis we identified a cytokine-related molecular signature in obese omental adipose tissue, characterized by a remarkable overexpression of interleukin (IL)-6, IL-1Î² and IL-10 associated with a concomitant increase in macrophage infiltration, which gradually increased in a body mass index-dependent manner. RNA profiling was conducted in 4 patients with morbid obesity and 4 control subjects using the Affymetrix Human Genome U219 expression array plate containing more than 36,000 transcripts and variants (Affymetrix, Inc., Santa Clara, CA).

2016-07-28 | E-GEOD-71415 | biostudies-arrayexpress

p38 Mitogen-Activated Protein Kinase Signals the Immunoresolving Actions of Resolvin D1 in Inflamed Human Visceral Adipose Tissue

Project description:Activation of the innate immune system leading to a persistent state of low-grade of tissue inflammation greatly influences the risk of developing metabolic complications associated with obesity. In this study, we characterized the inflammatory state in adipose tissue from obese patients and explored the potential of the specialized pro-resolving mediator (SPM) resolvin D1 (RvD1) to actively terminate inflammation and promote its resolution. By means of high-troughput transcritomic analysis we identified a cytokine-related molecular signature in obese omental adipose tissue, characterized by a remarkable overexpression of interleukin (IL)-6, IL-1β and IL-10 associated with a concomitant increase in macrophage infiltration, which gradually increased in a body mass index-dependent manner.

2016-07-28 | GSE71415 | GEO

Resolvin D1 attenuated liver injury caused by chronic ethanol and acute LPS challenge in mice

Project description:Alcohol-associated liver disease (ALD) is a major health problem with limited effective treatment options. Alcohol-associated hepatitis (AH) is a subset of severe ALD with a high rate of mortality due to infection, severe inflammation, and ultimately multi-organ failure. There is an urgent need for novel therapeutic approaches to alleviate the human suffering associated with this condition. Resolvin D1 (RvD1) promotes the resolution of inflammation and regulates immune responses. The current study aimed to test the therapeutic efficacy and mechanisms of RvD1-mediated effects on liver injury and inflammation in an experimental animal model that mimics severe AH in humans. Our data demonstrated that mice treated with RvD1 had attenuated liver injury and inflammation caused by EtOH and LPS exposure by limiting hepatic neutrophil accumulation and decreasing hepatic levels of pro-inflammatory cytokines. In addition, RvD1 treatment attenuated hepatic pyroptosis, an inflammatory form of cell death, via downregulation of pyroptosis-related genes such as GTPase family member b10 and guanylate binding protein 2, and reducing cleavage of caspase 11 and gasdermin-D. In vitro experiments with primary mouse hepatocytes and bone marrow-derived macrophages confirmed the effectiveness of RvD1 in the attenuation of pyroptosis. In summary, our data demonstrated that RvD1 treatment provided beneficial effects against liver injury and inflammation in an experimental animal model recapitulating features of severe AH in humans. Our results suggest that RvD1 may be a novel adjunct strategy to traditional therapeutic options for AH patients.

2023-09-05 | GSE220520 | GEO

Resolvin D1 attenuated liver injury caused by chronic ethanol and acute LPS challenge in mice

Project description:Resolvin D1 attenuated liver injury caused by chronic ethanol and acute LPS challenge in mice

| PRJNA910124 | ENA

Resolvin D1 Reduces Lung Infection and Inflammation Activating Resolution in Cystic Fibrosis.

Project description:Non-resolving lung inflammation and Pseudomonas aeruginosa infections are the underlying cause of morbidity and mortality in cystic fibrosis (CF). The endogenous lipid mediator resolvin (Rv) D1 is a potent regulator of resolution, and its roles, actions, and therapeutic potential in CF are of interest. Here, we investigated actions and efficacy of RvD1 in preclinical models of cystic fibrosis. Cftr knockout mice with chronic P. aeruginosa lung infection were treated with RvD1 to assess differences in lung bacterial load, inflammation, and tissue damage. Cells from volunteers with CF were treated with RvD1 during ex vivo infection with P. aeruginosa, and effects on phagocytosis and inflammatory signaling were determined. In CF mice, RvD1 reduced bacterial burden, neutrophil infiltration, and histological signs of lung pathology, improving clinical scores of diseases. Mechanistically, RvD1 increased macrophage-mediated bacterial and leukocyte clearance in vivo. The clinical significance of these findings is supported by actions in primary leukocytes and epithelial cells from volunteers with CF where RvD1 enhanced P. aeruginosa phagocytosis and reduced genes and proteins associated to NF-κB activation and leukocyte infiltration. Concentration of RvD1 in sputum from patients with CF was also inversely correlated to those of cytokines and chemokines involved in CF lung pathology. These findings demonstrate efficacy of RvD1 in enhancing resolution of lung inflammation and infections and provide proof of concept for its potential as a prototypic novel pro-resolutive therapeutic approach for CF.

| S-EPMC7247852 | biostudies-literature

A common polymorphism in the Intelectin-1 gene influences mucus plugging in severe asthma

Project description:By incompletely understood mechanisms, type 2 (T2) inflammation present in the airways of severe asthmatics drives the formation of pathologic mucus which leads to airway mucus plugging. Here we investigate the molecular role and clinical significance of intelectin-1 (ITLN-1) in the development of pathologic airway mucus in asthma. Through analyses of human airway epithelial cells we find that ITLN1 gene expression is highly induced by interleukin-13 (IL-13) in a subset of metaplastic MUC5AC+ mucus secretory cells, and that ITLN-1 protein is a secreted component of IL-13-induced mucus. Additionally, we find ITLN-1 protein binds the C-terminus of the MUC5AC mucin and that its deletion in airway epithelial cells partially reverses IL-13-induced mucostasis. Through analysis of nasal airway epithelial brushings, we find that ITLN1 is highly expressed in T2-high asthmatics, when compared to T2-low children. Furthermore, we demonstrate that ITLN1 gene expression is significantly reduced and ITLN-1 protein expression is lost through a common genetic variant that is associated with protection from the formation of mucus plugs in T2-high asthma. This work identifies one of the first biomarkers and targetable pathways for the treatment of mucus obstruction in asthma.

2024-04-04 | GSE254127 | GEO

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