Fungi implicated in the development of AFS are predominantly of the dematiaceous family, and include Alternaria, Curvularia, Bipolaris specifera, and Exserohilum species. Aspergillus was originally implicated but is now understood to account for only 10% to 20% of cases (4). The presence of these fungi is insufficient to cause disease, as these same fungi are cultured from the nasal mucus of healthy patients as well. It has been suggested that the pathology seen in susceptible individuals is the result of an allergic response to the fungal antigens. In support of this hypothesis, fungal-specific immediate-hypersensitivity skin testing is frequently positive. These patients have an elevated serum total IgE and fungal-specific IgG. Histologic analysis of allergic mucin shows a characteristic eosinophilic infiltrate, fungal hyphae, and Charcot-Leyden crystals within the eosinophils. The immune response results in local mucosal edema that causes obstruction of the involved sinus ostia, perpetuating the process.
Molecular investigations have uncovered further evidence in support of this model. Extracellular major basic protein (MBP) and neutrophil elastase have been detected within the allergic mucin. The presence of these proteins in high quantities is indicative of eosinophil and neutrophil activation (5). Local fungal-specific IgE and IgG can be demonstrated in the mucin of two-thirds of AFS cases, suggesting a role for locally produced IgE (6). In AFS, it is likely that germinating hyphae contained within the allergic mucin provide persistent IgE-mediated antigenic stimulation that drives the paranasal inflammation (3).
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