ABSTRACT
Allergic bronchopulmonary mycosis (ABPM) develops mainly in patients with asthma or cystic fibrosis via types I and III hypersensitivity reactions to filamentous fungi. Aspergillus spp., especially Aspergillus fumigatus, is the major causative fungus because of its small conidia, thermophilic hyphae, and ability to secrete serine proteases. The cardinal histological feature of ABPM is allergic (eosinophilic) mucin-harboring hyphae in the bronchi, for which the formation of extracellular DNA trap cell death (ETosis) of eosinophils induced by viable fungi is essential. Clinically, ABPM is characterized by peripheral blood eosinophilia, increased IgE levels in the serum, IgE and IgG antibodies specific for fungi, and characteristic radiographic findings; however, there are substantial differences in the clinical features of this disease between East and South Asian populations. Systemic corticosteroids and/or antifungal drugs effectively control acute diseases, but recurrences are quite common, and development of novel treatments are warranted to avoid adverse effects and emergence of drug-resistance due to prolonged treatment with corticosteroids and/or antifungal drugs.
Subject(s)
Humans , Acute Disease , Adrenal Cortex Hormones , Antibodies , Asian People , Aspergillus , Aspergillus fumigatus , Asthma , Bronchi , Cell Death , Cystic Fibrosis , Diagnosis , Eosinophilia , Eosinophils , Extracellular Traps , Fungi , Hypersensitivity , Hyphae , Immunoglobulin E , Immunoglobulin G , Invasive Pulmonary Aspergillosis , Recurrence , Serine Proteases , Spores, FungalABSTRACT
Previously, we reported that epigallocatechin 3-O-gallate (EGCg) has growth-inhibitory effect on clinical isolates of Candida species. In this study, we investigated the antifungal activity of EGCg and antifungal agents against thirty-five of dermatophytes clinically isolated by the international guidelines (M38-A2). All isolates exhibited good susceptibility to EGCg (MIC50, 2-4 microg/mL, MIC90, 4-8 microg/mL, and geometric mean (GM) MICs, 3.36-4 microg/mL) than those of fluconazole (MIC50, 2-16 microg/mL, MIC90, 4-32 microg/mL, and GM MICs, 3.45-25.8 microg/mL) and flucytosin (MIC50, MIC90, and GM MICs, >64 microg/mL), although they were less susceptible to other antifungal agents, such as amphotericin B, itraconazole, and miconazole. These activities of EGCg were approximately 4-fold higher than those of fluconazole, and were 4 to 16-fold higher than flucytosin. This result indicates that EGCg can inhibit pathogenic dermatophyte species. Therefore, we suggest that EGCg may be effectively used solely as a possible agent or combined with other antifungal agents for antifungal therapy in dermatophytosis.