ArticleFrontiers in immunology2025
Identification of a multiple DAMP scavenger mimicking the DAMP-binding site of TLR4 to ameliorate lethal sepsis.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Dahuang-mudanpi decoction mitigates ALI/ARDS pulmonary inflammation via multi-target regulation of HMGB1.Frontiers in pharmacology · 2026Article
- Dynamic trajectories of inflammatory biomarkers and post-stroke cognitive impairment: a comprehensive review of neuroimmune mechanisms, longitudinal modeling, and clinical translation.Frontiers in neurology · 2026Review
- Pharmacological intervention of the HMGB1-pCTS-L axis to ameliorate inflammatory diseases.Frontiers in immunology · 2026Review
- A novel molecule targeting neutrophil-mediated B-1a cell trogocytosis attenuates sepsis-induced acute lung injury.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. Current treatments are limited to source control and supportive care, underscoring the urgent need for novel therapeutic interventions. Endogenous molecules released from stressed or damaged cells, known as damage-associated molecular patterns (DAMPs), exacerbate inflammation, organ injury, and mortality in sepsis. In this study, we discovered a novel therapeutic compound, opsonic peptide 18 (OP18), designed to scavenge multiple DAMPs, including extracellular cold-inducible RNA-binding protein (eCIRP), high mobility group box 1 (HMGB1) and histone H3, by facilitating their clearance via macrophages. OP18 was developed by identifying a 15-amino acid (aa) binding site within the extracellular domain of Toll-like receptor 4 (TLR4) shared by eCIRP, HMGB1, and histone H3, then extending it with an α
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