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GEO accession GSE252465 is currently private and is scheduled to be released on Feb 07, 2026.

ABSTRACT: GEO accession GSE252465 is currently private and is scheduled to be released on Feb 07, 2026.

PROVIDER: PRJNA1060696 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27494900_1.fastq.gz	Fastqsanger.gz
	SRR27494900_2.fastq.gz	Fastqsanger.gz
	SRR27494901_1.fastq.gz	Fastqsanger.gz
	SRR27494901_2.fastq.gz	Fastqsanger.gz
	SRR27494902_1.fastq.gz	Fastqsanger.gz

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Early-stage idiopathic pulmonary fibrosis is characterized by bronchoalveolar accumulation of SPP1+ macrophages

Project description:Patients affected by idiopathic pulmonary fibrosis (IPF), a progressive chronic and eventually fatal lung disease with unknown causes, suffer from delayed diagnosis due to the lack of predictive markers for disease development. Prior studies focused on the cellular and transcriptomic changes found in lung tissue during established, often terminal, lung disease. In clinical routine, bronchoscopy is applied for diagnosis and staging of suspected IPF affected individuals, thus providing us with a clinically applicable window, to study the cellular and transcriptional changes within affected individuals. Here we study a patient collective consisting of 11 IPF affected individuals and 11 healthy controls. We investigate their single cell transcriptomic profile alongside their cellular surface phenotype of alveolar-resident immune cells. Single cell transcriptional analysis reveals early accumulation of SPP1+ macrophages (SPP1+M) within the alveolar space as an early cellular sign of IPF, in the absence of a decline in lung function. Early-stage IPF accumulated SPP1+M were characterized by high expression of lipid storage and handling genes, accumulation of intracellular cholesterol and expression of proinflammatory cytokine expression. In silico developmental trajectory analysis revealed that SPP1+M are likely derived from monocytes. Finally to confirm the clinical diagnostic value of SPP1+ M we developed a flow cytometry panel to rapidly identify and test for the presence of SPP1+ M in bronchoalveolar lavage samples and confirm our observation in an independent validation cohort. Taken together, we show that SPP1+ M are associated with early IPF pathogenesis in the absence of an obvious decline in lung function, thus providing a clinically valuable markers for easy diagnosis of early IPF in clinical practice.

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Proliferating SPP1/MERTK-expressing macrophages in idiopathic pulmonary fibrosis

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Project description:The pathogenesis of idiopathic pulmonary fibrosis is multifactorial and characterized by progressive fibrosis and excessive accumulation of extracellular matrix in the interstitium of the lung, and driven by an imbalance between anti-fibrotic and pro-fibrotic factors leading to collagen deposition. In the present study we wanted to identify proteins involved in these processes, and performed high-resolution proteomic profiling of bronchoalveolar lavage (BAL) from IPF patients and controls. The proteomic analysis of BAL demonstrated that the complement system was highly differentially regulated in IPF patients as compared with controls.

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Proteomic profiling of bronchoalveolar lavage fluid uncovers unique protein clusters linked to survival in idiopathic pulmonary fibrosis and interstitial pneumonia with autoimmune features

Project description:This study aimed to delineate molecular phenotypes of the lung microenvironment across idiopathic interestitial pneumonias, namely interstitial pneumonia with autoimmune features (IPAF)and idiopathic pulmonary fibrosis (IPF) through proteomic analysis of bronchoalveolar lavage fluid (BALF).

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Idiopathic pulmonary fibrosis bronchoalveolar lavage cells RNA-seq indicates macrophage expression of pro-inflammatory M1/M2 activation concomitant with radical species metabolism inhibition

Project description:Current concepts of idiopathic pulmonary fibrosis (IPF) are that microscopic injury drives alveolar epithelial cell dysregulated activation and epithelial mesenchymal transition, ensuing fibrocyte recruitment, fibroblast proliferation and ECM deposition. With the background that IPF is also characterized by chronic accumulation of activated alveolar macrophages (aMAC) in the lower respiratory tract, we assessed IPFaMAC gene expression to identify patterns of activation, by RNA-seq using Illumina platform. To this we evaluated a population of 7 normal smoking controls and 16 IPF smoking patients. All IPFs had abnormal lung function and bronchoalveolar lavage (BAL) showing >80% macrophage counts and augmented spontaneous O2 radical release. RNA was extracted from whole BAL cells. Reads were mapped onto the UCSC mRNA database (GRCh37/hg19 version), and transcripts were aggregated by gene symbol, obtaining a final 19,723 unique protein-coding gene ID list, used for further analysis.

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Proliferating SPP1/MERTK-expressing macrophages in idiopathic pulmonary fibrosis

Project description:A comprehensive understanding of the changes in gene expression in cell types involved in idiopathic pulmonary fibrosis (IPF) will shed light on the mechanisms underlying the loss of alveolar epithelial cells, and development of honeycomb cysts and fibroblastic foci. We sought to understand changes in IPF lung cell transcriptomes and gain insight into innate immune aspects of pathogenesis. We investigated IPF pathogenesis using single cell RNA-sequencing of fresh lung explants, comparing human IPF fibrotic lower lobes reflecting late disease, upper lobes reflecting early disease and normal lungs. IPF lower lobes showed increased fibroblasts, and basal, ciliated, goblet and club cells, but decreased alveolar epithelial cells, and marked alterations in inflammatory cells. We found three discrete macrophage subpopulations in normal and fibrotic lungs, one expressing monocyte markers, one highly expressing FABP4 and INHBA (FABP4hi), and one highly expressing SPP1 and MERTK (SPP1hi). SPP1hi macrophages in fibrotic lower lobes showed highly upregulated SPP1 and MERTK expression. Low-level local proliferation of SPP1hi macrophages in normal lungs was strikingly increased in IPF lungs. Co-localization and causal modeling supported the role for these highly proliferative SPP1hi macrophages in activation of IPF myofibroblasts in lung fibrosis. These data suggest SPP1hi macrophages contribute importantly to lung fibrosis in IPF, and that therapeutic strategies targeting MERTK and macrophage proliferation may show promise for treatment of this disease.

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Quantitative proteomic analysis of bronchoalveolar lavage fluid in West Highland white terriers with canine idiopathic pulmonary fibrosis C4PR_LIV

Project description:Canine idiopathic pulmonary fibrosis (CIPF) is a chronic, progressive, interstitial fibrosing lung disease, manifesting as cough, exercise intolerance and ultimately, dyspnea and respiratory failure. It mainly affects West Highland white terriers (WHWTs), lacks curable treatment and has a poor prognosis. Aspiration of gastroesophageal refluxate may play a role in the development of CIPF. In the first part of this study, we completed label-free quantitative proteomic analysis of bronchoalveolar lavage fluid (BALF) from CIPF and healthy WHWTs. In the second part, we evaluated potential protein markers of reflux aspiration from canine gastric juice and vomitus and evaluated whether these were present in BALF from the two groups.

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Characterization of Spp1-TAP and Mer2-TAP interactomes

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

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2020-04-22 | GSE145926 | GEO

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