Transcriptome sequencing of pancreas and adipose tissues in obesity-related alcohol-induced acute pancreatitis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA822805 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18590157_1.fastq.gz | Fastqsanger.gz | |||
| SRR18590157_2.fastq.gz | Fastqsanger.gz | |||
| SRR18590158_1.fastq.gz | Fastqsanger.gz | |||
| SRR18590158_2.fastq.gz | Fastqsanger.gz | |||
| SRR18590159_1.fastq.gz | Fastqsanger.gz |
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Project description:Acute pancreatitis (AP) is an acute inflammation of the pancreas, mainly caused by gallstones and alcohol, and driven by changes in communication between cells. Heparin-binding proteins (HBPs) of the plasma membrane and extracellular matrix play a central role in cell communication. Therefore, we used heparin affinity proteomics to identify the extracellular HBPs in mouse normal pancreas (NP) and in a caerulein mouse model of AP. Many new HBPs (460) were discovered more than doubling their total number to 883. A number of the new HBPs are proteins with well-characterised intracellular functions, e.g. NDUFS4, NDUFS6, but which also have a documented extracellular presence with potential ‘moonlighting’ roles. The HBPs form highly interconnected protein-protein interaction networks in both NP and AP, as well as globally. Thus, HBPs may represent the most interconnected set of extracellular proteins and so those with the greatest regulatory potential. HBPs in NP are associated with biological functions such as molecular transport, cellular movement and tissue architecture that underlie pancreatic homeostasis. However, in AP HBPs are additionally associated with processes such as acute phase response signalling, complement system and mitochondrial dysfunction. By virtue of their extracellular location and heparin binding property, HBPs are easily accessible and are potential biomarkers and drug targets in AP.
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Project description:Obesity is a known risk factor for diseases of the pancreas, including diabetes, pancreatic cancer and pancreatitis, but mechanisms remain unclear. To elucidate how obesity impacts pancreatic immune homeostasis, we performed spatial, transcriptomic and functional profiling of human pancreatic immune cells from obese and non-obese organ donors. Obesity was associated with higher density of tissue resident memory T-cells (TRM) in the exocrine pancreas which display high cytotoxic functions and aggregated around macrophages. Single cell sequencing of pancreatic macrophages revealed two main subsets - FOLR2+ CD11c- fetal-derived macrophages with pro-repair and immunoregulatory function and a FOLR2- CD11c+ monocyte-derived macrophages with greater T-cell interactions and pro-inflammatory function. In obesity, the pancreatic macrophage landscape shifts to lower predominance of FOLR2+ CD11c- macrophages and higher FOLR2- CD11c+ macrophages which interact selectively with the TRM and inflamed exocrine epithelium. Together, these results identify macrophage-T cell circuits and immune epithelial interactions that fuel chronic pancreatic inflammation in obesity – a potential unifying mechanism for obesity-related pancreatic diseases
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Project description:BACKGROUND & AIMS: Acinar cells produce digestive enzymes that impede transcriptomic characterization of the exocrine pancreas. Thus, single-cell RNA-sequencing (scRNA-seq) studies of the pancreas underrepresent acinar cells relative to histological expectations, and a robust approach to capture pancreatic cell responses in disease states is needed. We sought to innovate a method that overcomes these challenges to accelerate study of the pancreas in health and disease. METHODS: We introduce FixNCut, a scRNA-seq approach where tissue is reversibly fixed with dithiobis(succinimidyl propionate) prior to dissociation and single-cell preparation. We apply FixNCut to an established mouse model of acute pancreatitis, validate findings using GeoMx whole transcriptome atlas (WTA) profiling, and integrate our data with prior studies to benchmark our method in both mouse and human pancreas datasets. RESULTS: FixNCut achieves unprecedented definition of challenging pancreatic cells including acinar and immune populations in homeostasis and acute pancreatitis, and identifies changes in all major cell types during injury and recovery. We define the acinar transcriptome during homeostasis and acinar-to-ductal metaplasia and establish a unique gene set to measure deviation from normal acinar identity. We characterize pancreatic immune cells, and analysis of T-cell subsets reveals a polarization of the homeostatic pancreas towards type-2 immunity. We report immune responses during acute pancreatitis and recovery, including early neutrophil infiltration, expansion of dendritic cell subsets, and a substantial shift in the transcriptome of macrophages due to both resident macrophage activation and monocyte infiltration. CONCLUSIONS: FixNCut preserves pancreatic transcriptomes to uncover novel cell states during homeostasis and following pancreatitis, establishing a broadly applicable approach and reference atlas for study of pancreas biology and disease.
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