ArticleAllergy, asthma & immunology research2025
Platelet-Activating Factor Disrupts the Nasal Epithelial Barrier Independently of the Platelet-Activating Factor Receptor Pathway.
Article in Allergy, asthma & immunology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- ATP/P2X7 signaling as a potential predictive biomarker for early recurrence of nasal polyps: Correlation with inflammasome activation and epithelial barrier dysfunction.The World Allergy Organization journal · 2026Article
- Endothelial activation in thromboangiitis obliterans: mechanisms and therapeutic horizons.Frontiers in immunology · 2025Review
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Authors and funding
8 authors.
Funding
Abstract
purposePlatelet-activating factor (PAF) mediates nasal congestion and rhinorrhea by affecting vascular permeability, but the underlying mechanisms remain unclear. Here, we sought to explore the effect of PAF on the nasal epithelial barrier in chronic rhinosinusitis with nasal polyps (CRSwNP).
methodsHuman nasal epithelial cells (hNECs) were pre-treated with Apafant, a PAF receptor (PAFR) inhibitor, or MCC950, an NOD-like receptor protein 3 (NLRP3) inflammasome inhibitor, before PAF stimulation. The nasal epithelial barrier function was assessed by measuring the transepithelial electrical resistance (TER) and sodium fluorescein flux. Additionally, the expression of mRNAs and proteins of tight junctions were assessed.
resultsPAF significantly decreased TER and enhanced the fluorescein flux permeability in air-liquid interface cultures of hNECs, while also downregulating the expression of ZO-1, occludin, claudin-1, and claudin-4. However, the disruptive effect of PAF on the nasal epithelial barrier was attenuated by MCC950, but not by Apafant. Furthermore, MCC950 inhibited PAF-induced NLRP3 activation and its downstream molecules, including caspase-1, ASC, interleukin (IL)-1β, and IL-18.
conclusionsOur findings indicate that PAF has the potential to disrupt the nasal epithelial barrier in CRSwNP and may be linked to NLRP3 activation, while PAFR is not essential for this process. This discovery helps to explain why PAFR antagonists are ineffective in blocking PAF-mediated inflammation in clinical settings.
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