Figure 1. Altered epithelial barrier function contributes to type 2-mediated inflammation in chronic rhinosinusitis and nasal polyps. Several factors, including allergens, bacteria, viruses, and fungi can activate nasal epithelial cells to produce innate cytokines that activate type 2 innate lymphoid cells. IL-5 derived from these latter contributes to airway eosinophilia, whereas IL-13 acts directly on the epithelium to drive goblet cell metaplasia. IL-4 promotes IgE production by B cells, which causes mast cell and basophil activation. Mast cells activate fibroblasts to produce collagen fibers. In addition, mast cells produce mediators that can induce vasodilation and tissue edema. Nasal epithelial cells can also undergo epithelial-to-mesenchymal transition under hypoxia, as observed in chronic rhinosinusitis and nasal polyps. EMT, epithelial-to-mesenchymal transition; ILC2, type 2 innate lymphoid cell.
