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<p>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.</p>

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Crosstalk between airway epithelial cells and mast cells in airway inflammation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月5日

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  • Junfan Wang,
  • Yuting Liang,
  • Liting Wu,
  • Ting Xu,
  • Wenfang Zhuang,
  • Jia Li

摘要

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.