ArticleLife science alliance2021
Macrophages-induced IL-18-mediated eosinophilia promotes characteristics of pancreatic malignancy.
Article in Life science alliance, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Acinar-ductal metaplasia in pancreatitis and pancreatic ductal adenocarcinoma.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- IL-18-Mediated Tumor Immune Evasion.Current issues in molecular biology · 2026Review
- Recent Advances in Non-Invasive Blood Markers for Intraductal Papillary Mucinous Neoplasm Grading.Oncology research · 2026Review
- Unveiling the multidimensional cytokine landscape in acute pancreatitis.Frontiers in immunology · 2026Article
- Preoperative interleukin-17a as a predictor of acute pancreatitis after pancreaticoduodenectomy.World journal of gastrointestinal surgery · 2025Article
- Article
- Proteomics in pancreatic cancer.Biomarker research · 2025Review
- The role of inflammatory factors in the tumor microenvironment of pancreatic cancer.Frontiers in immunology · 2025Review
- Allergen-induced NLRP3/caspase1/IL-18 signaling initiate eosinophilic esophagitis and respective inhibitors protect disease pathogenesis.Communications biology · 2023Article
- Heparanase 2 (Hpa2)- a new player essential for pancreatic acinar cell differentiation.Cell death & disease · 2023Article
- In Vivo protection from SARS-CoV-2 infection by ATN-161 in k18-hACE2 transgenic mice.Life sciences · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Reports indicate that accumulated macrophages in the pancreas are responsible for promoting the pathogenesis of chronic pancreatitis (CP). Recently, macrophage-secreted cytokines have been implicated in promoting pancreatic acinar-to-ductal metaplasia (ADM). This study aims to establish the role of accumulated macrophage-activated NLRP3-IL-18-eosinophil mechanistic pathway in promoting several characteristics of pancreatic malignancy in CP. We report that in a murine model of pancreatic cancer (PC), accumulated macrophages are the source of NLRP3-regulated IL-18, which promotes eosinophilic inflammation-mediated accumulation to periductal mucin and collagen, including the formation of ADM, pancreatic intraepithelial neoplasia (PanINs), and intraductal papillary mucinous neoplasm. Most importantly, we show improved malignant characteristics with reduced levels of oncogenes in an anti-IL-18 neutralized and IL-18 gene deficient murine model of CP. Last, human biopsies validated that NLRP3-IL-18-induced eosinophils accumulate near the ducts, showing PanINs formation in PC. Taken together, we present the evidence on the role of IL-18-induced eosinophilia in the development of PC phenotype like ADM, PanINs, and ductal cell differentiation in inflammation-induced CP.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.