Modeling Human Airway Epithelial Barrier Penetration Using Birch Bet v 1 and Alder Aln g 1 Pollen Allergens During Sensitization Process

TL;DR

This study compares how two pollen allergens interact with human airway cells, showing how they may trigger allergic reactions.

Contribution

The study reveals novel insights into how Aln g 1 and Bet v 1 allergens affect epithelial barrier function and immune signaling during sensitization.

Findings

Both Aln g 1 and Bet v 1 allergens disrupt liposomes modeling pulmonary surfactant.

Aln g 1 and Bet v 1 show similar transport efficiency through an artificial epithelial barrier.

Aln g 1 upregulates immune-related genes like IL-33, TSLP, IL-1β, and CXCL8 in epithelial cells.

Abstract

Pollen allergy is rated as a major public health problem, causing significant morbidity and adversely affecting the quality of people’s lives. The airway epithelium serves as the first line of defense in the respiratory system, playing a crucial role in orchestrating immune responses to allergens. In this work, we studied the important transport steps in the major alder pollen allergen Aln g 1 through the human airway epithelium in comparison with those of the birch pollen allergen Bet v 1. Using fluorescence spectroscopy, we showed that both allergens can destroy liposomes with a composition modeling the adult human pulmonary surfactant. Using a polarized Calu-3 monolayer, we showed similar efficiencies of Aln g 1 and Bet v 1 transport through the artificial epithelial barrier. Using qPCR, we showed that Aln g 1 upregulates the expression of IL-33, TSLP, IL-1β, CXCL8 in epithelial cells, playing an important role in the sensitization process. The obtained results may improve our understanding of the primary sensitization mechanisms with the involvement of the PR-10 family of lipid-binding allergens.

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