ArticleAmerican journal of translational research2025
Dectin-1 participates in β-glucan- or PMA-induced neutrophil extracellular trap formation during antifungal defense.
Article in American journal of translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- Neutrophil extracellular traps in antifungal immunity: mechanisms, dual roles, regulatory networks, and clinical perspectives.Frontiers in cellular and infection microbiology · 2026Review
- Neutrophil Extracellular Traps in Sepsis and Sepsis-Related Organ Dysfunction.ImmunoTargets and therapy · 2025Review
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Authors and funding
8 authors.
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Abstract
objectivesThe formation of neutrophil extracellular traps (NETs) plays a crucial role in neutrophil-mediated defense against fungal infections and has become a hot topic of immunological research. This study aimed to investigate whether high expression of Dectin-1, a key pattern recognition receptor, contributes to NET formation in response to fungal pathogens.
methodsHuman neutrophils were isolated and characterized, then stimulated with cell wall β-glucan to induce NET formation. Phorbol 12-myristate 13-acetate (PMA), a diacylglycerol mimetic, was used as a positive control. Dectin-1 antibody was used to determine the functional significance of Dectin-1 in the formation of NETs. NET formation was detected by Sytox Green staining, myeloperoxidase (MPO) and neutrophil elastase (NE) immunofluorescence staining, and western blot analysis. The relative kits, 2',7'-dichlorodihydrofluorescein diacetate staining and MitoSOX Red staining were used to determine the mechanism of Dectin-1 induced NET formation.
resultsDectin-1 was overexpressed in β-glucan- and PMA-treated neutrophils. Dectin-1 deficiency reduced NET formation, accompanied by decreased Sytox Green fluorescence, lower levels of dsDNA content, and decreased expression of NE, MPO and citrullinated histone H3 (H3Cit). Dectin-1-mediated NET formation was dependent on reactive oxygen species (ROS) produced by NADPH oxidase (NOX), NOX2 protein and mitochondrial superoxide. Moreover, up-regulated Dectin-1 expression activated the extracellular regulated protein kinases (ERK) and p38 MAPK pathways, which were critical for the induction of NETs.
conclusionDectin-1 promotes NET formation in neutrophils stimulated by β-glucan or PMA through activation of the ERK and p38 signaling pathways, which might contribute to defense against fungal pathogens.
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