Exploring serum sST2 and miR-223 as potential biomarkers of disease activity and clinical response to SLIT in HDM-induced allergic rhinitis.

Soluble suppression of tumorigenicity 2 (sST2), a decoy receptor of interleukin-33 (IL-33), is involved in allergic inflammation and may serve as a biomarker in allergic rhinitis (AR). MicroRNA-223 (miR-223) has also been implicated in allergic inflammation. To investigate serum sST2 and miR-223 as potential biomarkers of disease activity and treatment-associated changes in patients with house dust mite (HDM)-induced moderate-to-severe allergic rhinitis (MSAR) undergoing sublingual immunotherapy (SLIT). This study included 54 patients with moderate-to-severe AR (MSAR) and 54 healthy controls (HC). Serum sST2, total IgE, HDM-specific IgE, and eosinophil counts were measured. Serum miR-223 relative expression was assessed using real-time PCR. Clinical severity was assessed using the total nasal symptom score (TNSS) and visual analogue scale (VAS). MSAR patients received SLIT for 6 months. Treatment response was defined as a ≥ 30% reduction in TNSS from baseline. Serum sST2 and miR-223 were significantly higher in MSAR patients than in healthy controls (p < 0.001). sST2 correlated positively with HDM-specific IgE and eosinophil counts and decreased significantly after six months of treatment (p < 0.001). Post-treatment sST2 was lower in responders, whereas baseline sST2 did not differ significantly between groups. ROC analysis showed good discrimination of MSAR from HC for sST2 (AUC = 0.933) and miR-223 (AUC ≈ 0.96). Serum sST2 and miR-223 show promising potential as candidate biomarkers of HDM-induced MSAR. The decrease in sST2 after treatment suggests its potential value for monitoring treatment-associated changes. Further studies are needed to validate these findings.Trial registration Retrospectively registered on ClinicalTrials.gov, registered at 25/2/ 2026, Identifier (NCT07436208). Registered at: https://clinicaltrials.gov/study/NCT07436208.