Increased glucose transporter 1 contributes to epithelial barrier dysfunction in allergic rhinitis

Epithelial barrier impairment is a characteristic pathological hallmark of allergic rhinitis (AR), yet the mechanisms contributing to this dysfunction remain incompletely understood. Our aim is to assess the impact of glucose transporter 1 (GLUT1) on epithelial barrier function in AR.

We performed proteomics analysis on nasal mucosa from AR patients and healthy controls (HCs) to identify differential proteins, which were validated using immunofluorescence, western blotting, and RT-qPCR. Nasal epithelial cells from HCs were isolated to evaluate house dust mite (HDM)-induced changes in GLUT1 expression and regulatory mechanisms. An AR mouse model was constructed to examine the effects of GLUT1 inhibition on nasal inflammation and barrier function.

Tissue proteomics analysis revealed a distinct protein expression profile in AR patients compared with HCs, with GLUT1 identified as the most upregulated protein. Cohort validation demonstrated significantly elevated GLUT1 expression in the AR group, predominantly localized in epithelial cells. Moreover, GLUT1 mRNA levels showed a positive correlation with visual analogue scales and total nasal symptom scores, and a negative correlation with tissue ZO-1 and occludin expressions. In vitro studies indicated that HDM stimulation enhanced GLUT1 expression and reduced ZO-1 and occludin levels in nasal epithelial cells in a dose-dependent manner. Treatment with a GLUT1 inhibitor effectively restored ZO-1 and occludin expressions. Animal model experiments further confirmed that GLUT1 inhibition alleviated nasal inflammation and improved mucosal barrier function.

AR displays a distinct tissue-specific protein expression profile, with enhanced GLUT1 levels associated with disease severity and epithelial barrier dysfunction. Inhibition of GLUT1 has been shown to reduce nasal inflammation and improve epithelial barrier function in AR.