OBJECTIVE: Fungus may contribute to the development and exacerbation of allergic airway diseases. Several studies have demonstrated the presence of humoral immune responses to fungi, including Alternaria and Aspergillus, in patients with nasal polyposis, asthma, or rhinitis. The purpose of this study was to evaluate the role of Alternaria- and Aspergillus-specific IgE antibodies in allergic inflammation of adenoid tissue. METHODS: Thirty-nine atopic subjects who were sensitized to more than one common aeroallergen and 39 non-atopic subjects undergoing adenotonsillectomy were recruited. The Phadia ImmunoCAP was used to quantify total IgE, Alternaria- and Aspergillus-specific IgE, eosinophil cationic protein (ECP), and mast cell tryptase in adenoid tissue homogenates. Alternaria- and Aspergillus-specific IgE were detected in the adenoid tissues from some of the subjects (37.2% and 24.4%, respectively) without systemic sensitization to common airborne fungi. RESULTS: Both Alternaria- and Aspergillus-specific IgE were more prevalent in adenoid tissues from atopic children (48.7% and 38.5%, respectively) than in tissues from non-atopic children (25.6% and 10.3%, respectively). Subjects with high Alternaria-specific IgE level showed significantly higher serum and adenoid total IgE and adenoid ECP and tryptase than those without specific IgE. Alternaria-specific IgE levels were significantly correlated with serum and adenoid total IgE and with tryptase and ECP levels in adenoid tissue. CONCLUSIONS: Adenoid tissues from atopic and non-atopic children displayed local IgE-mediated hypersensitivity to fungi in the absence of systemic fungal hypersensitivity. Locally-produced Alternaria-specific IgE may contribute to mast cell and eosinophil activation, especially in the presence of tissue eosinophilia.
OBJECTIVE: Fungus may contribute to the development and exacerbation of allergic airway diseases. Several studies have demonstrated the presence of humoral immune responses to fungi, including Alternaria and Aspergillus, in patients with nasal polyposis, asthma, or rhinitis. The purpose of this study was to evaluate the role of Alternaria- and Aspergillus-specific IgE antibodies in allergic inflammation of adenoid tissue. METHODS: Thirty-nine atopic subjects who were sensitized to more than one common aeroallergen and 39 non-atopic subjects undergoing adenotonsillectomy were recruited. The Phadia ImmunoCAP was used to quantify total IgE, Alternaria- and Aspergillus-specific IgE, eosinophil cationic protein (ECP), and mast cell tryptase in adenoid tissue homogenates. Alternaria- and Aspergillus-specific IgE were detected in the adenoid tissues from some of the subjects (37.2% and 24.4%, respectively) without systemic sensitization to common airborne fungi. RESULTS: Both Alternaria- and Aspergillus-specific IgE were more prevalent in adenoid tissues from atopic children (48.7% and 38.5%, respectively) than in tissues from non-atopic children (25.6% and 10.3%, respectively). Subjects with high Alternaria-specific IgE level showed significantly higher serum and adenoid total IgE and adenoid ECP and tryptase than those without specific IgE. Alternaria-specific IgE levels were significantly correlated with serum and adenoid total IgE and with tryptase and ECP levels in adenoid tissue. CONCLUSIONS: Adenoid tissues from atopic and non-atopic children displayed local IgE-mediated hypersensitivity to fungi in the absence of systemic fungal hypersensitivity. Locally-produced Alternaria-specific IgE may contribute to mast cell and eosinophil activation, especially in the presence of tissue eosinophilia.