{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Li T"],"funding":["National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases R01DK118065"],"pagination":["461"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11273487"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(7)"],"pubmed_abstract":["Fibroblast heterogeneity remains undefined in eosinophilic esophagitis (EoE), an allergic inflammatory disorder complicated by fibrosis. We utilized publicly available single-cell RNA sequencing data (GSE201153) of EoE esophageal biopsies to identify fibroblast sub-populations, related transcriptomes, disease status-specific pathways and cell-cell interactions. IL13-treated fibroblast cultures were used to model active disease. At least 2 fibroblast populations were identified, F_A and F_B. Several genes including <i>ACTA2</i> were more enriched in F_A. F_B percentage was greater than F_A and epithelial-mesenchymal transition upregulated in F_B vs. F_A in active and remission EoE. Epithelial-mesenchymal transition was also upregulated in F_B in active vs. remission EoE and TNF-α signaling via NFKB was downregulated in F_A. IL-13 treatment upregulated ECM-related genes more profoundly in ACTA2- fibroblasts than ACTA2+ myofibroblasts. After proliferating epithelial cells, F_B and F_A contributed most to cell-cell communication networks. ECM-Receptor interaction strength was stronger than secreted or cell-cell contact signaling in active vs. remission EoE and significant ligand-receptor pairs were driven mostly by F_B. This unbiased analysis identifies at least 2 fibroblast sub-populations in EoE in vivo, distinguished in part by <i>ACTA2</i>. Fibroblasts play a critical role in cell-cell interactions in EoE, most profoundly via ECM-receptor signaling via the F_B sub-group."],"journal":["Biology"],"pubmed_title":["Differential Contributions of Fibroblast Subpopulations to Intercellular Communication in Eosinophilic Esophagitis."],"pmcid":["PMC11273487"],"funding_grant_id":["National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases R01DK118065"],"pubmed_authors":["Khalatbari A","Li T","Shao L","Castle JD","Salomon M","Shaker A"],"additional_accession":[]},"is_claimable":false,"name":"Differential Contributions of Fibroblast Subpopulations to Intercellular Communication in Eosinophilic Esophagitis.","description":"Fibroblast heterogeneity remains undefined in eosinophilic esophagitis (EoE), an allergic inflammatory disorder complicated by fibrosis. We utilized publicly available single-cell RNA sequencing data (GSE201153) of EoE esophageal biopsies to identify fibroblast sub-populations, related transcriptomes, disease status-specific pathways and cell-cell interactions. IL13-treated fibroblast cultures were used to model active disease. At least 2 fibroblast populations were identified, F_A and F_B. Several genes including <i>ACTA2</i> were more enriched in F_A. F_B percentage was greater than F_A and epithelial-mesenchymal transition upregulated in F_B vs. F_A in active and remission EoE. Epithelial-mesenchymal transition was also upregulated in F_B in active vs. remission EoE and TNF-α signaling via NFKB was downregulated in F_A. IL-13 treatment upregulated ECM-related genes more profoundly in ACTA2- fibroblasts than ACTA2+ myofibroblasts. After proliferating epithelial cells, F_B and F_A contributed most to cell-cell communication networks. ECM-Receptor interaction strength was stronger than secreted or cell-cell contact signaling in active vs. remission EoE and significant ligand-receptor pairs were driven mostly by F_B. This unbiased analysis identifies at least 2 fibroblast sub-populations in EoE in vivo, distinguished in part by <i>ACTA2</i>. Fibroblasts play a critical role in cell-cell interactions in EoE, most profoundly via ECM-receptor signaling via the F_B sub-group.","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jun","modification":"2024-11-09T16:54:56.427Z","creation":"2024-11-09T16:54:56.427Z"},"accession":"S-EPMC11273487","cross_references":{"pubmed":["39056656"],"doi":["10.3390/biology13070461"]}}