Activation of Eosinophils with Airborne Fungi.
- Author:
Seung Heon SHIN
1
;
Jeong Kyu KIM
;
Hirohito KITA
Author Information
1. Department of Otolaryngology, College of Medicine, Daegu Catholic University, Daegu, Korea.
- Publication Type:Original Article
- Keywords:
Sinusitis;
Fungi;
Eosinophils;
Protease inhibitors
- MeSH:
Alternaria;
Antigens, Fungal;
Aspergillus;
Candida;
Cladosporium;
Eosinophil-Derived Neurotoxin;
Eosinophils*;
Epithelial Cells;
Fungi*;
Healthy Volunteers;
Hot Temperature;
Hyphae;
Mucins;
Protease Inhibitors;
Serine;
Serine Proteases;
Serine Proteinase Inhibitors;
Sinusitis;
Superoxides
- From:Korean Journal of Otolaryngology - Head and Neck Surgery
2004;47(6):549-553
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVES: Allergic fungal sinusitis is characterized by allergic mucin which includes eosinophils and fungal hyphae. But we don't know why eosinophils are accumulated at the nasal secretion and activated, so authors tried to explain the pathophysiologic function of eosinophils by directly stimulating eosinophils with fungal antigens. SUBJECTS AND METHOD: Eosinophils were isolated from healthy volunteers and stimulated with extracts from 5 common fungal species (Alternaria, Aspergillus, Candida, Cladosporium, and Penicillium). Superoxide production and eosinophil derived neurotoxin (EDN) were measured to determine whether fungi activated eosinophils. An inhibition study was done using serine and cystein protease inhibitors. RESULTS: When cultured with fungal antigens, eosinophils produced superoxide by Alternaria and Cladosporium but only Alternaria induced EDN production. Serine protease inhibitors (PMSF, Pefabloc?) and heat treatment of fungi significantly inhibited the activation of eosinophils but the cystein protease inhibitor (E-64) wasn't inhibited. CONCLUSION: Eosinophils are directly activated by Alternaria and their activity was inhibited by serine protease inhibitors. In AFS, fungal serine proteases may activate eosinophils which play important roles in the pathogenesis of AFS, resulting in the destruction of fungi and respiratory epithelial cells.
