ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Wedelolactone, a Novel TLR2 Agonist, Promotes Neutrophil Differentiation and Ameliorates Neutropenia: A Multi-Omics Approach to Unravel the Mechanism.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Cichorium intybus L. polysaccharide improves growth performance and colonic barrier function in weaned piglets via the microbiota-HDCA-TGR5-Akt-NF-κB signaling axis: validation by FMT and in vitro models.Journal of animal science and biotechnology · 2026Article
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Authors and funding
17 authors.
Funding
Abstract
Neutropenia, a common complication in cancer patients undergoing radiotherapy, heightens the risk of infection and mortality, with limited treatment options. This study investigates wedelolactone (WED), a natural coumarin, as a potential therapeutic agent. WED is found to promote neutrophil differentiation and enhance bactericidal function in vitro. Its in vivo efficacy is validated in radiation-induced neutropenic mouse and zebrafish models, where it facilitates rapid recovery of leukocyte and neutrophil levels. An integrated approach using the GEO database, RNA sequencing, molecular docking, and Drug Affinity Responsive Target Stability (DARTS) assays identifies TLR2 and its downstream MAPK signaling pathway as essential for WED's anti-neutropenic effects. DARTS confirms significant binding of WED to TLR2. Knockdown of TLR2 with siRNA or inhibition of TLR2 with C29 reduces WED-induced neutrophil differentiation, MEK1/2 and ERK1/2 phosphorylation, and expression of transcription factors (PU.1, CEBPβ). Similarly, ERK1/2 inhibition by SCH772984 impairs WED-induced neutrophil differentiation and bactericidal activity, decreasing PU.1 and CEBPβ expression without affecting TLR2 levels. These findings position TLR2 as a key therapeutic target for neutropenia, with WED effectively promoting neutrophil differentiation via TLR2 and MEK/ERK pathway activation. This study highlights the therapeutic potential of targeting TLR2 to alleviate neutropenia and underscores the utility of a multi-omics approach in uncovering drug mechanisms.
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Registered trials
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