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γδ+ T cell-derived IL-17A stimulates airway epithelial/stromal cells to secrete G-CSF, promoting lung-specific pathogenic Siglec-F+ neutrophil development in PPE-induced emphysema

ABSTRACT: γδ+ T cell-derived IL-17A stimulates airway epithelial/stromal cells to secrete G-CSF, promoting lung-specific pathogenic Siglec-F+ neutrophil development in PPE-induced emphysema

PROVIDER: PRJNA1263770 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33598630.fastq.gz	Fastqsanger.gz
	SRR33598631.fastq.gz	Fastqsanger.gz
	SRR33598632.fastq.gz	Fastqsanger.gz
	SRR33598633.fastq.gz	Fastqsanger.gz
	SRR33598634.fastq.gz	Fastqsanger.gz

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γδ+ T cell-derived IL-17A stimulates airway epithelial/stromal cells to secrete G-CSF, promoting lung-specific pathogenic Siglec-F+ neutrophil development in PPE-induced emphysema

Project description:Neutrophils play a pivotal role in the progression of IL-17-mediated airway inflammation, but the mechanisms underlying their pathological differentiation remain poorly understood. In this study, we identified a distinct population of lung-specific pathogenic Siglec-F+ neutrophils in a porcine pancreatic elastase (PPE)-induced mouse model of emphysema. These Siglec-F+ neutrophils exhibited enhanced phagocytic activity, increased extracellular trap formation, and elevated production of pro-inflammatory cytokines, alongside reduced IL-10 levels, compared to conventional neutrophils. During the early phase of acute inflammation following PPE instillation, IL-17A levels in the lung increased, primarily driven by γδ+ T cells. IL-17A stimulated lung epithelial/stromal cells to secrete granulocyte colony-stimulating factor (G-CSF), which promoted the differentiation of Siglec-F+ neutrophils via the JAK2/STAT3 pathway, PI3K-independent mTOR, and p38 MAPK signaling pathways. Neutralizing G-CSF or inhibiting JAK2/STAT3, mTOR or p38 MAPK signaling significantly suppressed Siglec-F+ neutrophil development, resulting in alleviation of emphysematous symptoms. Our findings underscore the crucial role of Siglec-F+ neutrophils in the pathogenesis of PPE-induced emphysema and suggest that targeting the IL-17A/G-CSF axis or G-CSF receptor downstream signaling pathways may represent a promising therapeutic strategy for treating emphysema.

2025-05-23 | GSE297403 | GEO

Testosterone deficiency altered mortality and the expression profile of protease inhibitors in an elastase-induced mouse model of emphysema

Project description:To evaluate the effect of testosterone on the pathophysiology of COPD, we created porcine pancreas elastase (PPE)-induced emphysema mouse model in sham or orchiectomized (ORX) mice [sham/PBS, sham/PPE, ORX/PBS, and ORX/PPE]. We performed microarray analysis to compare the gene expression levels in the lungs of each mice group. The results demonstrated that the levels of genes encoding protease inhibitor activity in ORX/PPE mice were lower than those in sham/PPE mice.

2023-06-24 | GSE153148 | GEO

PE/PPE MTB study

Project description:PE/PPE MTB study

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Type-I interferon inducible genes 26 weeks after mCMV infection in Siglec-H wt and Siglec-H ko mice and their non infected controls

Project description:Type I interferons are critical anti-viral cytokines during virus infections and have also been implicated in the pathogenesis of systemic lupus erythematosus (SLE). The secretion of type I interferon of pDCs is modulated by Siglec-H, a DAP12 associated receptor on pDCs. We showed that Siglec-H deficient pDCs produce more of the type I interferon IFN-Î± in vitro and that Siglec-H ko mice produce more IFN-Î± after murine cytomegalovirus (mCMV) infection in vivo, leading to efficient clearance of the virus. Furthermore, ageing Siglec-H ko mice showed a mild form of systemic autoimmunity. In contrast, Siglec-H ko mice developed a severe form of systemic lupus-like autoimmune disease with strong kidney nephritis several weeks after a single mCMV infection. This induction of systemic autoimmune disease after virus infection in Siglec-H ko mice was accompanied by a type I interferon signature and fully dependent on type I interferon signaling. These results show that Siglec-H normally serves as modulator of type I interferon responses after infection with a persistent virus and thereby prevents induction of autoimmune disease. For microarray experiments gene expression profiles of total splenic cells from two wt and Siglec-H ko mice 26 weeks after infection with luciferase expressing murine Cytomegalovirus (5x105 pfu) or from two uninfected wt and Siglec-H ko control mice were analyzed

2016-03-16 | E-GEOD-79248 | biostudies-arrayexpress

Gene signature profiles in lung tissues of wild type mice or Has2 heterozygous deficient mice stimulated with porcine pancreatic elastase

Project description:Chronic obstructive pulmonary disease (COPD) is an inflammatory lung condition primarily caused by prolonged exposure to harmful substances, such as cigarette smoke. Hyaluronic acid synthase 2 (HAS2) synthesizes high-molecular-weight hyaluronic acid (HMW-HA), believed to have anti-inflammatory properties. Previous studies have suggested that HAS2 dysfunction may exacerbate COPD. However, the specific impact of HAS2 on pulmonary emphysema progression remains unclear. In this study, we tested the hypothesis that HAS2 dysfunction worsens airway inflammation and emphysema in mouse COPD model. Has2 heterozygous-deficient (Has2+/-) mice and their wild-type (WT) littermates have been evaluated in a porcine pancreatic elastase (PPE)-induced COPD model. Following PPE administration, Has2+/- mice exhibited a significant increase in total cell and neutrophil counts in BALF samples compared to WT mice. Has2+/- mice demonstrated enhanced emphysema development on histological analyses, with higher values of mean linear intercept relative to wild-type mice. Elastase-stimulated Has2+/- mice also demonstrated increased G-CSF level and TGF-β attenuation in lung. RNA-seq analysis suggested that PPE stimulation promotes HMW-HA synthesis and TGF-β signaling. GO analysis using Has2+/- mice-specific DEGs showed that genes associated with pathways that "negative regulation of transforming growth factor beta receptor signaling pathway" were activated after PPE administration. This study demonstrates that Has2 dysfunction exacerbates neutrophilic airway inflammation and emphysema, underscoring the protective role of HAS2 in a PPE induced emphysema model. The exacerbated response appears to involve G-CSF and TGF-β-related signaling pathways. These findings may contribute to the development of novel therapeutic strategies for COPD management.

2025-09-26 | GSE304417 | GEO

Eosinophils promote lung emphysema via CTSL

Project description:Patients with chronic obstructive pulmonary disease (COPD) having higher blood eosinophil levels exhibit worse lung function and more severe emphysema, implying the potential role of eosinophils in emphysema development. However, the specific mechanism underlying eosinophil-mediated emphysema development is not fully elucidated. In this study, single-cell RNA sequencing was used to identify eosinophil subgroups in mouse models of asthma and emphysema and analyze their functions. Analysis of the accumulated eosinophils revealed differential transcriptomes between the mouse lungs of elastase-induced emphysema and ovalbumin-induced asthma., Eosinophil depletion alleviated elastase-induced emphysema. Notably, eosinophil-derived cathepsin L (CTSL) degraded the extracellular matrix (ECM), causing emphysema in the pulmonary tissue. Eosinophils were positively correlated with serum CTSL levels, which were increased in patients with emphysema than in those without emphysema. Collectively, these results suggest that CTSL expression in eosinophils plays an important role in ECM degradation and remodeling and is related to emphysema in patients with COPD. Therefore, eosinophil-derived CTSL may serve as a potential therapeutic target for patients with emphysema.

2023-10-17 | GSE237749 | GEO

Murine Abdominal Aortic Aneurysm, PPE Model - In Vivo Modulation of miRNA-24 (Day 7)

Project description:Transcriptional profiling of infrarenal aortic tissue from Male 10-week-old C57BL/6J mice after AAA-induction with porcine pancreatic elastase, compared with sham-operated saline-injected mice. One day after AAA-induction, the mice were injected intraperitoneally with either lentiviral packaged miR-24 antagomir (anti-miR-24) or miR-24 mimic (pre-miR-24), or a scrambled microRNA control (scr-miR). Aortic samples were obtained 7 days after operation. The goal was to examine gene expression in developing AAA in this model, and to compare the effects of scr-miR, anti-miR-24 and pre-miR-24. Four condition experiment, one infrarenal aorta per array. Sham vs. scr-miR-PPE vs. anti-miR-24-PPE vs. pre-miR-24-PPE, all harvested at Day 7 post-operatively. After QC, the final analysis group (uploaded here) consisted of 18 arrays: Sham-Saline-treated (4 arrays), scr-miR-PPE-treated (5 arrays); pre-miR-24-PPE-treated (3 arrays); and anti-miR-24-PPE-treated (6 arrays).

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Project description:Identification of human brain ligand for the microglial inhibitory receptors Siglec-3 (CD33) and Siglec-8

2022-03-07 | PXD032064 | JPOST Repository

MicroRNA transciptional profiling in murine abdominal aortic aneurysm (AAA), porcine pancreatic elastase (PPE) model - Day 7

Project description:We sought to identify differentially regulated microRNAs in infrarenal mouse aortic tissue after AAA-induction with PPE, compared with sham-operated mice. This treatment leads to rapid development of infrarenal aortic aneurysms with significant diameter differences observed by Day 7. We found 41 miRNAs were up-regulated with aneurysm and 37 down-regulated at p<0.05, which were also altered by >1.5-fold. Utilizing the PPE infusion model, we induced AAA in Male 10-week-old C57/Bl6 mice, 7 days after AAA-induction with PPE. One array per mouse, 5 mice per group, two groups (PPE and sham).

2014-08-31 | E-GEOD-51226 | biostudies-arrayexpress

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