Crosstalk between airway epithelial cells and mast cells in airway inflammation
Junfan Wang, Yuting Liang, Liting Wu, Ting Xu, Wenfang Zhuang, Jia Li
Abstract
Airway epithelial cells (AECs) and mast cells (MCs) are pivotal initiators and amplifiers of airway inflammation, orchestrating a dynamic crosstalk that drives pathological hyperreactivity in respiratory diseases. AECs, as the frontline barrier, detect pathogens and allergens, releasing cytokines (e.g., IL-33, TSLP) and chemokines to activate neighboring MCs. Conversely, MC-derived proteases (tryptase, chymase) and mediators (histamine, leukotrienes) disrupt epithelial junctions (e.g., E-cadherin, occludin), exacerbating barrier dysfunction and perpetuating cycles of inflammation. This reciprocal interaction establishes a molecular hub for 'hyperinflammation' in asthma, chronic obstructive pulmonary disease (COPD), and viral infections, while also contributing to pathological processes such as airway remodeling, fibrosis, and epithelial-mesenchymal transition (EMT). Therefore, elucidating the synergistic mechanisms underlying AEC-MC crosstalk is critically important. This review synthesizes emerging insights into AEC-MC crosstalk, emphasizing context-specific mechanisms in viral, allergic, and chronic inflammatory settings, and provide suggestions for future research directions.