FIGURE 3.

Schematic view of T2 eosinophilic airway inflammation in the pathophysiology of asthma. Allergens or epithelial damage activates dendritic cells that secrete cytokines, such as IL-4, leading to Th2 differentiation. Th2 lymphocytes secrete IL-4 and IL-13 amplifying Th2 proliferation and promoting the generation of IgE by B lymphocytes. Th2 cells also secrete IL-5, the most important cytokine for eosinophil recruitment. IL-13 secreted mainly by eosinophils activates iNOS expression increasing NO levels in the airways and consequently F_ENO. NO, in turn, is also involved in Th2 differentiation. Moreover, iNOS expression on epithelial cells could be also enhanced by oxidants, pollutants, or proinflammatory stimuli such as TNF-α or INF-γ. Chronic eosinophil inflammation is involved in tissue airway remodeling and bronchial obstruction caused by an increase of airway smooth muscle mass, epithelial cell hyperplasia, goblet cell metaplasia, mucus overproduction, and basement membrane thickening caused by deposition of extracellular matrix proteins. The image has been created with Biorender.