Background: The factors responsible for inducing or maintaining airway inflammation are poorly understood. Various studies have focussed on the mechanisms leading to allergic airway inflammation in patients with asthma and rhinitis. The observation of local airway inflammation in nonallergic patients with asthma or rhinitis, including those with nasal polyposis, suggest that non-IgE–related mechanisms exist that may lead to airway inflammation. Various lines of evidence suggest that epithelial cells may participate in local inflammation of the airways.

Objective: This study focused on the interaction of airway epithelial cells with clinically relevant inhalant allergen extracts in vitro.

Methods: Cultures of airway epithelial cells were exposed to mite, Timothy grass pollen, and birch pollen extracts. Production of IL-8, IL-6, monocyte-chemotactic protein-1 (MCP-1), and granulocyte-macrophage colony-stimulating factor and cell detachment were monitored while protease inhibitors and chromatography techniques were applied to identify the factors responsible for these effects.

Results: With the mite extracts, cytokine production and cell detachment was largely dependent on protease activity. With the pollen extracts, cytokine production without cell detachment seemed to be independent of protease activity.

Conclusion: These findings support the view that epithelial cells may contribute to the pathogenesis of airway disease by their interaction with inhalant allergen extracts. Furthermore, allergen extracts may enhance airway inflammation by means other than their IgE-binding activity through both protease-dependent and protease-independent mechanisms. (J Allergy Clin Immunol 1998;102:75-85.)