Preliminary evidence for IRAK2 as a potential biomarker and in vitro pro-inflammatory mediator in allergic rhinitis

Allergic rhinitis (AR) is a common chronic nasal mucosal inflammation with limited treatment options. IRAK2 regulates allergic airway inflammation, but its expression, clinical value, and mechanism in AR remain unexplored. This study screened AR-related candidate genes using bioinformatics, verified serum IRAK2 expression and its clinical significance in AR patients, and explored its functional mechanism in vitro. GEO datasets were used to screen differentially expressed genes and candidate genes related to AR. Serum samples were collected from 100 AR patients and 100 healthy controls. Serum IRAK2 levels were detected, and correlation analysis, ROC curve analysis and logistic regression analysis were performed. LPS‑stimulated human nasal epithelial cells were applied to explore the effects of IRAK2 on inflammation, oxidative stress, NF‑κB and p38 MAPK pathway-related protein expression, and epithelial barrier function. Bioinformatics analysis identified IRAK2 as a candidate gene in AR. Serum IRAK2 was significantly upregulated in AR patients, and it was positively correlated with total IgE and TNSS scores. It showed favorable diagnostic accuracy for AR and showed an independent statistical association with AR. In vitro, IRAK2 modulated the expression of NF‑κB and p38 MAPK proteins, accompanied by elevated inflammatory and oxidative stress levels as well as altered tight junction protein expression. IRAK2 shows potential as a diagnostic biomarker for AR, based on preliminary clinical evidence. In the LPS‑induced in vitro model, IRAK2 may function as a pro‑inflammatory mediator to drive inflammatory responses with involvement of the NF‑κB and p38 MAPK pathways, but these mechanistic findings are limited to the cell model and require in vivo validation. Not applicable.