The Microbiota in Chronic Pancreatitis
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ABSTRACT:
PROVIDER: PRJEB78535 | ENA |
REPOSITORIES: ENA
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Project description:Chronic pancreatitis (CP) is a pathogenically complex fibro-inflammatory disorder of the pancreas. Our understanding of CP pathogenesis is partly limited by the incomplete characterization of pancreatic cell types. Here, we performed single-cell RNA sequencing on 3,386 cells from the pancreas of one control mouse and mice with caerulein-induced CP. These data provides a preliminary description of the single-cell transcriptome profiles of mouse pancreata and accurately demonstrates the characteristics of pancreatic ductal cells in CP.
2022-06-30 | GSE204844 | GEO
Project description:A frequently used experimental model of chronic pancreatitis (PC) recapitulating human disease is repeated injection of cerulein to mice. We found that two common substrains of C57BL/6 , C56BL/6J (Jackson) and C57BL/6NHsd (Harlan), exhibit different degree of CP with C57BL/6J beeing more susceptible to repetitive cerulein induced CP. The goal of this study was to identify genes associated with CP and also to identify genes differentially regulated between two substrains as candidates for the CP progression. RNAs were isolated from the pancreas of 8-week old Jackson and Harlan mice after the cerulein induction of chronic pancreatitis and hybridized on Affymetrix microarrays. Saline injected mice were used as controls. Three mice from each experimental and control groups were used in the experiment.
2012-10-10 | E-GEOD-41418 | biostudies-arrayexpress
Project description:A frequently used experimental model of chronic pancreatitis (PC) recapitulating human disease is repeated injection of cerulein to mice. We found that two common substrains of C57BL/6 , C56BL/6J (Jackson) and C57BL/6NHsd (Harlan), exhibit different degree of CP with C57BL/6J beeing more susceptible to repetitive cerulein induced CP. The goal of this study was to identify genes associated with CP and also to identify genes differentially regulated between two substrains as candidates for the CP progression.
2012-10-10 | GSE41418 | GEO
Project description:We used 10x Genomics Single Cell 3’v3.1 scRNA sequencing to investigate the cellular heterogeneity in chronic pancreatitis using pancreases of three CP mice. Mice were induced by daily subcutaneous re-injections of caerulein for 28 days
2022-06-22 | GSE182971 | GEO
Project description:827 human miRNA standard human panel Plasma derived extracellular vesicles (EV)/exosomes can serve as markers of cell damage/disease but can also have therapeutic utility depending on the nature of their cargo, such as miRNA. Currently there are challenges and lack of innovations regarding early diagnosis and therapeutic options within different aspects of management of patients suffering from chronic pancreatitis (CP). Use of exosomes as biomarkers for pancreatic health, and/or or as adjuvant therapy would make a difference in management of these patients. To explore the feasibility of this approach, we characterized the miRNA cargo of exosomes purified from CP patients, and compared it to those from healthy participants. Methods: EVs were isolated from plasma of 15 CP patients and 10 healthy controls. Nanoparticle Tracking Analysis was used to determine frequency and size while NanoString technology was used to characterize the miRNA cargo. Relevant clinical parameters were correlated with these EV/exosome characteristics. Results: ~30 miRNA species were identified to have significantly (p<0.05) different expression in exosomes from individuals with CP compared to healthy individuals; ~40 miRNA were differentially expressed in exosomes from pre-diabetic versus non-diabetic CP patients. miR-579-3p, while exhibiting significantly lower (~16-fold) expression in exosomes from CP compared to healthy individuals and lower (~24-fold) in CP narcotic users compared to the less severe CP in non-users, is actually enriched (~32-fold) within exosomes in pre-diabetic CP patients compared to non-diabetic CP patients. A unique pattern was identified in female CP patients. Conclusions: These first of a kind data support the prospect of using a bioinformatics approach to assess pancreatic health, and their therapeutic potential in CP patients.
2021-04-29 | GSE173514 | GEO
Project description:Age-standardized incidence rates for pancreatic cancer (PC) in men have increased by 25% from 1957 to 2011 in Finland. The average age of diagnosis for PC is 69 years in Nordic males, whereas the average age of diagnosis of chronic pancreatitis (CP) is 40-50 years, but the cases overlap in age. By radiology the evaluation of a pancreatic mass, i.e. the differential diagnosis between CP and PC is often difficult. Preoperative needle biopsies are difficult to obtain and are demanding to interpret. New blood based biomarkers are needed. The accuracy of the only established biomarker for PC, CA 19-9 is rather poor in differentiating between benign and malignant mass of the pancreas. In this study, we have performed mass spectrometry HDMSE analysis of serum samples from patients with chronic pancreatitis and pancreatic cancer. We have quantified 652 proteins and performed detailed statistical analysis such as principal component analysis, orthogonal partial least square discriminant analysis and receiver operating curve analysis.
2017-06-09 | PXD005144 | Pride
Project description:Humanized PRSS1 transgenic mice were constructed and treated with caerulein to mimic the development of human AP and CP. Potential regulatory proteins in pancreatitis were screened by proteomics using pancreatic tissues of PRSS1 AP mice.
2021-09-09 | PXD016651 | Pride
Project description:Peripheral blood was collected from 87 patients with acute pancreatitis (AP) of varying severity (Mild=57, Moderately-Severe=20, Severe=10) within 24 hours of presentation to the hospital and from 32 healthy controls. RNA-Seq was performed to identify changes in expression in severe AP cf. mild, moderately-severe, and healthy controls.
2022-03-01 | GSE194331 | GEO
Project description:Purpose: Chronic pancreatitis (CP) is considered an irreversible fibroinflammatory pancreatic disease with no active FDA approved therapy. Due to difficulty in accessing pancreas tissues, little is known about local immune responses in human CP. Here we attempted to uncover the disease-specific immune responses in pancreata from two different etiologies of CP (hereditary and idiopathic CP) compared with those from non-diseased controls by using CITE-seq and scTCR-seq. Methods: We performed cellular indexing of transcriptomes and epitopes by sequencing (CITE-Seq) and T cell receptor sequencing of pancreatic immune cells isolated from organ donors (n=3) and CP patients (Hereditary CP, n=5; Idiopathic CP, n=4) who underwent total pancreatectomy. Results: Deep single-cell sequencing revealed distinct immune characteristics and a significantly enriched CCR6+ CD4+ T cells in hereditary compared with idiopathic CP. In hereditary CP, a reduction in T cell clonality was observed due to the increased CD4+ T (Th) cells that replaced tissue resident CD8+ T cells. Lineage tracing analysis with scRNA/TCR-seq data also unveiled unique interactions between CCR6+ Th and Th1 subsets, and TCR clustering analysis showed unique common antigen binding motifs in hereditary CP. In addition, we observed a significant upregulation of the CCR6 ligand (CCL20) among monocytes in hereditary CP as compared with those in idiopathic CP. The functional significance of the CCR6 expression in CD4+ T cells was confirmed by flow cytometry and migration assay. Conclusions: Our approaches with integrative single-cell analyses unveiled distinct pancreatic immune signatures and pathways between different etiologies of CP. Our study specifically unveiled pancreas-specific immune crosstalks through a CCR6-CCL20 axis that might be leveraged as a potential future target in human hereditary CP
2021-09-01 | GSE165045 | GEO
Project description:Excessive Hedgehog (Hh) signaling activity contributes to fibrosis in multiple organs, however, its role in pancreatic stellate cell (PSC) activation and fibrosis development during chronic pancreatitis (CP) remains unclear. We demonstrate that GLI2 is upregulated in activated PSCs from CP patients and animal models. Specific deletion of Gli2, but not Smo, significantly alleviated fibrosis in CP models, indicating that CP is driven by non-canonical Hh signaling. Experiments on culture-activated primary PSCs reveal early nuclear translocation and increased GLI2 expression promptly after in vitro culture, with GLI2 being essential for PSC activation. SMO inhibition only reduces GLI2 activation in the short term, while activation of GLI2 by TGF-β/SMAD3 signaling explains the SMO-independent mechanisms leading to Hh activation in PSCs. Altogether, our data demonstrate the activation of the non-canonical Hh pathway in PSCs and indicate that GLI2 represents a promising therapeutic target for CP.
2024-11-13 | GSE281427 | GEO