ArticleFrontiers in immunology2024
Neutrophil-fibroblast crosstalk drives immunofibrosis in Crohn's disease through IFNα pathway.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- High-throughput chemical screen identifies epothilone B in modulating inflammatory bowel disease by triggering neutrophil apoptosis.Genes & diseases · 2027Article
- Cellular crosstalk of fibroblast-myofibroblast transition in intestinal homeostasis and disease.Biomarker research · 2026Review
- Emerging evidence of neutrophil extracellular traps in essential hypertension and target organ damage: pathophysiological insights and therapeutic implications.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Review
- Identification of IL1RN, MUC1, and SERPINA1 as key NET-related biomarkers in ulcerative colitis-associated intestinal fibrosis via bioinformatics and experimental validation.BMC gastroenterology · 2026Article
- Regulation of calcium homeostasis by S100A12 drives NETosis in chronic kidney disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Intestinal subepithelial myofibroblasts in inflammatory bowel disease: fibroblast heterogeneity, fibrosis, and therapeutic targeting.Frontiers in medicine · 2026Review
- Peptidylarginine Deiminases: An Overview of Recent Advances in Citrullination Research.International journal of molecular sciences · 2025Review
- Integrative bioinformatics and machine learning approaches identify inflammation-related genes and drug candidates for future preclinical validation in ischemic stroke.BMC neurology · 2025Article
- The role of neutrophils in the pathophysiology of inflammatory bowel diseases.Periodontology 2000 · 2025Review
- Neutrophils and NETs in Pathophysiology and Treatment of Inflammatory Bowel Disease.International journal of molecular sciences · 2025Review
- Transcriptomic analysis reveals shared deregulated neutrophil responses in COVID-19 and idiopathic pulmonary fibrosis.Respiratory research · 2025Article
- Therapeutic potential of Janus kinase inhibitors for the management of fibrosis in inflammatory bowel disease.Journal of Crohn's & colitis · 2025Review
- Interleukin-8/Matrix Metalloproteinase-9 Axis Impairs Wound Healing in Type 2 Diabetes through Neutrophil Extracellular Traps-Fibroblast Crosstalk.European journal of immunology · 2025Article
- Anemia in diabetes mellitus: Pathogenetic aspects and the value of early erythropoietin therapy.Metabolism open · 2025Review
- The Cell-Specific Effects of JAK1 Inhibitors in Ulcerative Colitis.Journal of clinical medicine · 2025Review
- The role of fibroblast-neutrophil crosstalk in the pathogenesis of inflammatory diseases: a multi-tissue perspective.Frontiers in immunology · 2025Review
- Identification and validation of shared biomarkers and drug repurposing in psoriasis and Crohn's disease: integrating bioinformatics, machine learning, and experimental approaches.Frontiers in immunology · 2025Article
- Neutrophil-Fibroblast Crosstalk Drives Immunofibrosis in Sequelae of Pelvic Inflammatory Disease Through Neutrophil Extracellular Traps.Mediators of inflammation · 2025Article
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21 authors.
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Abstract
Introduction: Crohn's disease (CD) is characterized by chronic inflammation and intestinal fibrosis leading to lifelong complications. However, the disease pathogenesis remains elusive, and the therapeutic options are limited. Here, we investigated the interaction between neutrophils and intestinal fibroblasts in the development of CD immunofibrosis, a disease mechanism predisposing to inflammatory and fibrotic complications. Methods: Peripheral neutrophils, enriched neutrophil extracellular traps (eNETs), serum, primary intestinal fibroblasts (PIFs) and intestinal biopsies from CD, ulcerative colitis (UC) patients, and healthy individuals (HI), were studied. Transcriptome analysis of neutrophils, multi-cytokine profiling and cell-based functional assays at mRNA/protein level were performed. Results: Compared to UC, PIFs from CD patients, independently to the presence of strictures, displayed a distinct pro-fibrotic phenotype characterized by negative Krüppellike Factor-2 (KLF2) and increased cellular communication network factor-2 (CCN2) expression leading to collagen production. In both UC and CD, PIFs-derived IL-8 acted as a culprit chemoattractant for neutrophils in the intestine, where CD neutrophils were accumulated close to fibrotic lesions. Functionally, only CD neutrophils via eNETs induced a CD-like phenotype in HI PIFs, suggesting their fibrotic plasticity. High IFNa in serum and IFΝ-responsive signature in peripheral neutrophils were observed in CD, distinguishing it from UC. Moreover, CD serum stimulated the release of fibrogenic eNETs from neutrophils in an IFNa-dependent manner, suggesting the priming role of IFNa in circulating neutrophils. Inhibition of eNETs or JAK signaling in neutrophils or PIFs prevented the neutrophil-mediated fibrotic effect on PIFs. Furthermore, both serum IFNa levels and mRNA levels of key IFN signaling components in neutrophils were wellcorrelated with CD severity. Conclusions: This study reveals the important role of the IFNa/neutrophil/fibroblast axis in CD immunofibrosis, suggesting candidate biomarkers and putative therapeutic targets.
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