INTERACTIONS BETWEEN INHALANT ALLERGEN EXTRACTS AND AIRWAY EPITHELIAL-CELLS - EFFECT ON CYTOKINE PRODUCTION AND CELL DETACHMENT

Citation
Jfc. Tomee et al., INTERACTIONS BETWEEN INHALANT ALLERGEN EXTRACTS AND AIRWAY EPITHELIAL-CELLS - EFFECT ON CYTOKINE PRODUCTION AND CELL DETACHMENT, Journal of allergy and clinical immunology, 102(1), 1998, pp. 75-85
Citations number
44
Categorie Soggetti
Immunology,Allergy
ISSN journal
00916749
Volume
102
Issue
1
Year of publication
1998
Pages
75 - 85
Database
ISI
SICI code
0091-6749(1998)102:1<75:IBIAEA>2.0.ZU;2-K
Abstract
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 wit h asthma and rhinitis. The observation of local airway inflammation in nonallergic patients with asthma ol rhinitis, including those with na sal polyposis, suggest that non-IgE-related mechanisms exist that may Lead to airway inflammation. Various lines of evidence suggest that ep ithelial cells may participate in local inflammation of the airways. O bjective: This study focused on the interaction of airway epithelial c ells with clinically relevant inhalant allergen extracts in vitro. Met hods: Cultures of airway epithelial cells were exposed to mite, Timoth y grass pollen, and birch pollen extracts. Production of IL-8, IL-6, m onocyte-chemotactic protein-1 (MCP-1), and granulocyte-macrophage colo ny-stimulating factor and cell detachment were monitored while proteas e inhibitors and chromatography techniques were applied to identify th e factors responsible fur these effects. Results: With the mite extrac ts, cytokine production and cell detachment was largely dependent on p rotease activity. With the pollen extracts, cytokine production withou t cell detachment seemed to be independent of protease activity. Concl usion: These findings support the view that epithelial cells may contr ibute 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 th rough both protease-dependent and protease-independent mechanisms.