ArticleFrontiers in cell and developmental biology2025
IL-6 trans-signaling in cystic fibrosis bronchial cells potentiates TNF-α-driven ICAM-1 expression.
Article in Frontiers in cell and developmental biology, 2025. 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.
- The Involvement of MicroRNAs in Innate Immunity and Cystic Fibrosis Lung Disease: A Narrative Review.Current issues in molecular biology · 2026Review
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7 authors.
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Abstract
Introduction: Methods: sIL-6Ra expression was measured by ELISA in plasma samples from pwCF at baseline and during exacerbations. IL-6 signalling was investigate in CF and non-CF cell lines using immunoblotting of STAT3 phosphorylation. ICAM-1 cell surface expression was determined using flow cytometry. Results: We show that pwCF had higher sIL-6Rα levels in their plasma during PEx, suggestive of IL-6 trans-signaling. Furthermore, we show that a CF bronchial cell line is hyper-responsive to both classic and trans-signaling, with the higher levels of activation occurring during trans-signaling when compared to two non-CF cell lines. Discussion: Our data unveiled that ICAM-1, which promotes neutrophil adhesion, is upregulated by the combination of TNF-α and IL-6 signaling in CF bronchial cells. Interestingly, soluble IL-6R (sIL-6Rα) protects IL-6 from degradation by bacterial proteases. Therefore, we suggest that strategies which target IL-6 trans-signaling may alleviate ICAM-1 mediated neutrophil adhesion and reduce subsequent lung damage in PEx.
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