ArticleInternational journal of biological sciences2025
Macrophage Extracellular Traps Modulate the Compensatory Anti-inflammatory Response Syndrome through IL-33/ST2 Signaling in Severe Acute Pancreatitis.
Article in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Digoxin Alleviates Osteoarthritis by Inhibiting Macrophage Extracellular Trap Formation via Disruption of the LSP1-SOD1 Interaction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Macrophage programming in systemic sclerosis: Niches, networks, and translational horizons.Seminars in immunopathology · 2026Review
- Review
- Baicalin ameliorates acute pancreatitis through inhibiting the activation of cGAS/STING signaling pathway.Molecular biology reports · 2026Article
- From suspected necrotizing fasciitis to diagnosed drug-induced fever: a diagnostic maze and reflections on anti-infection management in a case of postoperative fever after femoral fracture.Frontiers in medicine · 2026Article
- Post-translational modification crosstalk in acute pancreatitis: linking acinar stress to innate immune amplification and tissue repair.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
17 authors.
Funding
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Abstract
Severe acute pancreatitis (SAP) is characterized by biphasic systemic inflammation, progressing from initial pro-inflammatory systemic inflammatory response syndrome (SIRS) to subsequent immunosuppressive compensatory anti-inflammatory response syndrome (CARS), which increases infection risks and predicts poor prognosis. Using a pancreatic duct ligation and caerulein-induced SAP murine model, we demonstrate that macrophage extracellular traps (METs) play a pivotal role in immune regulation. Mechanistically, acinar cell activation of the cGAS-STING pathway triggers pyroptosis-mediated IL-33 release. METs subsequently process IL-33 into highly bioactive isoforms through METs-derived proteases (including MMP-12), thereby initiating ST2 receptor-mediated type-2 immune responses. Clinical validation revealed elevated serum METs marker and IL-33 levels in SAP patients. Therapeutic interventions with DNase I and Cl-amidine significantly attenuated IL-33 release, Th2 cell activation, and disease severity in experimental models. Our findings establish METs as critical regulators of SAP-associated CARS and propose METs inhibition as a promising therapeutic strategy for SAP management.
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