Fungal-Induced Inflammation and Nasal Polyps

Airborne fungi are present in the nasal mucus of chronic rhinosinusitis (CRS) patients and normal healthy controls. Especially Alternaria induces the production of cytokines by epithelial cells (IL-33), inducing lymphocytes to release IL-13 and IL-5, which are crucial for the eosinophilic inflammation, occurring only in CRS patients but not in healthy controls. Preceding fungi induce an eosinophilic tissue airway inflammation and resulting nasal obstruction, which is in contrast to a neutrophilic response to bacteria. Eosinophils, in CRS mucus, target fungi in the mucus with CRS and nasal polyps. Fungal antigens also cause activation and degranulation of human eosinophils via the beta-2 integrin on the CD11b receptor, resulting in eosinophilic major basic protein (MBP) release and epithelial damage. Asperin sensitivity and the development of an IgE-mediated allergy Th2 shifting) can now be linked to fungal exposure. Anti IL-13 antibody treatment (dupilumab) is the first immunologic therapy approved for CRS with nasal polyps.