Abstract

Rationale Ragweed pollen, a clinically important and major aeroallergen, elicits bronchial airway inflammation. The inflammatory process involves changes in permeability with resulting edema, which can occur in asthma. There is little documentation investigating the mechanisms by which ragweed pollen causes changes in bronchial airway permeability. We sought to investigate the mechanisms by which ragweed pollen causes increased permeability in bronchial airway epithelial cells (BAECs). Methods We used enzyme-linked immunosorbent assay (ELISA) to estimate pollen-induced production of vascular endothelial growth factor (VEGF, also called vascular permeability factor) by BAECs. E-cadherin was visualized by immunofluorescent staining. We used fluorescent microscopy to visualize gap formation between BAECs. Pollen-induced changes in BAEC barrier function was estimated by measuring electrical resistance, using an Electrical Cell substrate Impedance-sensing System (ECIS). Results Ragweed pollen induced VEGF production in BAECs in a time-dependent manner. E-cadherin expression was significantly decreased in BAECs exposed to ragweed pollen. Ragweed pollen caused gap formation between BAECs in a time-dependent manner. Electrical resistance across the BAEC barrier was significantly decreased in pollen-exposed BAECs. Conclusions These data suggest that ragweed pollen induces VEGF production and down-regulation of E-cadherin, leading to gap formation between BAECs, which ultimately affects bronchial epithelial barrier function, thus causing increased bronchial airway permeability. This provides for a greater understanding of the mechanisms by which ragweed pollen causes airway inflammation, which is important in the pathophysiology of asthma.

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