GRK2408/TP12 - Th2 cell-dependent effects on the airway epithelial barrier during chronic asthma

Allergic asthma is characterized by chronic inflammation and airway remodeling, which involves epithelial barrier dysfunction, fibrosis, goblet cell hyperplasia/metaplasia, smooth muscle thickening and increased endothelial permeability (Lambrecht & Hammad, 2015). Repetitive chronic exposure to allergens such as from HDM mediates a dysregulation of the airway epithelia including alveolar type II cells (AECsII) (Heijink et al., 2020). This cumulates in Th2 cell activation and the amplification of asthmatic airway inflammation. However, how the intercellular communication between alveolar epithelial cells and Th2 cells contributes to the fixation of especially chronic asthmatic airway inflammation is still not fully understood. We hypothesize that in chronic asthma, metabolites provide a specific metabolic environment within the lung, which favors chronic inflammation and fixation of the disease by changing the epithelial barrier.