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Quantitative Analysis Reveals IL-17A Widens Nasal Epithelial Tight Junction Gaps via AMPK in Allergic Rhinitis
Huijun Qiu1, Junhai Chen2, Lijing Li3
1Department of Otorhinolaryngology-Head and Neck Surgery, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China; Department of Allergy, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China; Department of Otolaryngology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Background:
Allergic rhinitis (AR) is a chronic IgE-mediated inflammatory disease characterized by nasal epithelial barrier dysfunction. Interleukin-17A (IL-17A) has been implicated in epithelial barrier disruption, but its role in regulating nasal epithelial tight junctions (TJs) remains unclear.
Objective:
To investigate the effects of IL-17A on nasal epithelial TJs integrity and determine whether adenosine monophosphate-activated protein kinase (AMPK) signaling mediates IL-17A-induced barrier dysfunction in AR.
Methods:
Inferior turbinate tissues from patients with AR and healthy controls were analyzed by transmission electron microscopy, quantitative PCR, western blotting, and immunofluorescence. Human nasal epithelial cells cultured at an air-liquid interface were stimulated with IL-17A for 28 days. TJs integrity was assessed by transepithelial electrical resistance, fluorescein isothiocyanate-dextran permeability, and automated ImageJ-based quantification of TJs morphology. Bulk RNA sequencing was performed, and AMPK activity was modulated using AICAR and Compound C.
Results:
AR tissues exhibited disrupted TJs and suppressed AMPK activity. IL-17A expression was elevated and negatively correlated with TJs protein levels. In human nasal epithelial cells, IL-17A reduced TJs protein expression, decreased transepithelial electrical resistance, increased paracellular permeability, and widened intercellular spaces. Transcriptomic analysis demonstrated suppression of AMPK signaling after IL-17A stimulation. Activation of AMPK with AICAR restored TJs expression and improved barrier function.
Conclusion:
IL-17A impairs nasal epithelial barrier integrity by inhibiting AMPK signaling, whereas AMPK activation rescues TJs structure and function, identifying the IL-17A/AMPK axis as a potential therapeutic target in allergic rhinitis.
