Elevated S100A8 in nasal mucosa correlates with epithelial barrier dysfunction in allergic rhinitis

Area of Science:

• Immunology
• Cell Biology
• Allergy Research

Background:

• Epithelial barrier dysfunction is key in allergic rhinitis (AR) pathogenesis.
• The role of S100A8 in AR-induced barrier disruption requires further investigation.

Purpose of the Study:

• To investigate S100A8 expression in AR patients.
• To explore the association between S100A8 and nasal epithelial barrier dysfunction in AR.

Main Methods:

• Assessed S100A8 and tight junction protein expression (ZO-1, E-cadherin, occludin) in nasal tissues from AR patients and controls using Immunofluorescence, Western Blot, and RT-qPCR.
• Correlated S100A8 levels with AR severity scores (VAS, TNSS).
• Investigated S100A8's role in House Dust Mite (HDM)-induced barrier disruption in human nasal epithelial cells (HNECs) by silencing S100A8 with siRNA.

Main Results:

• S100A8 expression was significantly higher in AR patients compared to controls, correlating positively with symptom severity.
• Reduced expression of tight junction proteins (ZO-1, E-cadherin, occludin) was observed in AR patients, negatively correlating with S100A8 levels.
• HDM stimulation increased S100A8 and decreased tight junction proteins in HNECs; S100A8 silencing restored barrier protein expression.

Conclusions:

• S100A8 is upregulated in AR, linked to disease severity and epithelial barrier defects.
• Targeting S100A8 presents a potential therapeutic strategy for preserving nasal barrier integrity in AR.