ArticleFrontiers in immunology2019
TLR3 Ligand PolyI:C Prevents Acute Pancreatitis Through the Interferon-β/Interferon-α/β Receptor Signaling Pathway in a Caerulein-Induced Pancreatitis Mouse Model.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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12 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Putative molecular targets for vitamin A in neutralizing oxidative stress in acute and chronic pancreatitis - a systematic review.Naunyn-Schmiedeberg's archives of pharmacology · 2023Pooled it
- Diagnostic value of neutrophil/lymphocyte ratio, platelet/lymphocyte ratio and systemic immune-inflammation index for predicting the severity of acute pancreatitis.BMC gastroenterology · 2025Article
- Naa10p impairs PGC-1α/Pparγ2 interaction to inhibit mitochondrial protection in pancreatitis.Journal of cell communication and signaling · 2025Article
- Structural and Functional Characteristics of TLR19 in Barbel Chub Compared to TLR19 in Grass Carp.International journal of molecular sciences · 2025Article
- diABZI and poly(I:C) inhibit osteoclastic bone resorption by inducing IRF7 and IFIT3.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Article
- PFKFB3 controls acinar IP3R-mediated Ca2+ overload to regulate acute pancreatitis severity.JCI insight · 2024Article
- Revealing Prdx4 as a potential diagnostic and therapeutic target for acute pancreatitis based on machine learning analysis.BMC medical genomics · 2024Article
- Identifying the ceRNA Regulatory Network in Early-Stage Acute Pancreatitis and Investigating the Therapeutic Potential of NEAT1 in Mouse Models.Journal of inflammation research · 2024Article
- LincRNA-EPS alleviates severe acute pancreatitis by suppressing HMGB1-triggered inflammation in pancreatic macrophages.Immunology · 2021Article
- Wip1 Aggravates the Cerulein-Induced Cell Autophagy and Inflammatory Injury by Targeting STING/TBK1/IRF3 in Acute Pancreatitis.Inflammation · 2021Article
- Systemic Immune-Inflammation Index (SII) Can Be an Early Indicator for Predicting the Severity of Acute Pancreatitis: A Retrospective Study.International journal of general medicine · 2021Article
- Necrostatin‑1 protects mice from acute lung injury by suppressing necroptosis and reactive oxygen species.Molecular medicine reports · 2020Article
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11 authors at 6 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Acute pancreatitis (AP) is a common and devastating inflammatory disorder of the pancreas. However, there are still no effective treatments available for the disease. Therefore, it is important to discover new therapeutic targets and strategies for better treatment and prognosis of AP patients. Toll-like receptor 3 (TLR3) ligand polyI:C is a double-stranded RNA mimic that can be used as an immune stimulant. Our current study indicates that polyI:C exerted excellent anti-inflammatory effects in a caerulein-induced AP mouse model and taurocholate-induced pancreatic acinar cell line injury model. We found that polyI:C triggers type I interferon (IFN) production and downstream IFN-α/β receptor (IFNAR)-dependent signaling, which play key roles in protecting the pancreas from inflammatory injury. Knockout of IFN-β and IFNAR in mice abolished the preventive effects of polyI:C on caerulein-induced AP symptoms, which include pancreatic edema, neutrophil infiltration, the accumulation of reactive oxygen species (ROS), and inflammatory gene expression. Treating pancreatic acinar 266-6 cells with an IFNAR inhibitor, which blocks the interaction between type I IFN and IFNAR, diminishes the downregulation of oxidative stress by polyI:C. Additionally, a subsequent transcriptome analysis on the role of polyI:C in treating pancreatitis suggested that chemotaxis of neutrophils and the production of ROS were inhibited by polyI:C in the pancreases damaged by caerulein injection. Thus, polyI:C may act as a type I IFN inducer to alleviate AP, and it has the potential to be a promising therapeutic agent used at the early stages of AP.
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