ArticleArchives of microbiology2025
The immune response of upper and lower airway epithelial cells to Aspergillus fumigatus and Candida albicans-derived β-glucan in Th17 type cytokine environment.
Article in Archives of microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
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Authors and funding
5 authors.
Funding
Abstract
The fungal cell wall component β-glucan activates inflammation via the Dectin-1 receptor and IL-17 coordinates the antifungal immunity. However, the molecular crosstalk between IL-17, Dectin-1, and β-glucan in epithelial cells and fungal immunity remains unclear. We investigated the impact of A.fumigatus-derived β-glucan (AFBG) and C.albicans-derived β-glucan (CABG) on Dectin-1 and cytokines in nasal epithelial cells (NECs) and bronchial epithelial cells (BECs) in the presence of IL-17. CABG reduced BEC viability more than AFBG despite similar Dectin-1 expression. IL-17 reduced β-glucan-dependent Dectin-1 expression in NECs but increased it in BECs after 12 h. AFBG synergized with IL-17, enhancing pro-inflammatory cytokines and chemokine expressions. IL-6 and IL-8 production increased in the presence of IL-17. Th17 cytokine influenced the Dectin-1 response to fungal β-glucan in NECs and BECs, impacting the initiation and nature of epithelial cell reactions to AFBG and CABG. Uncovering the molecular mechanisms of fungal β-glucans in the respiratory tract could lead to novel strategies for preventing fungal diseases.
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Registered trials
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