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探索血清sST2和miR-223作为屋尘螨诱导的过敏性鼻炎疾病活动度和舌下免疫治疗临床反应的潜在生物标志物

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

临床研究鼻科IF 4.8Q1

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中文摘要

可溶性肿瘤抑制因子2(sST2)是白细胞介素-33(IL-33)的诱饵受体,参与过敏性炎症,可能作为过敏性鼻炎(AR)的生物标志物。微小RNA-223(miR-223)也与过敏性炎症有关。本研究旨在探讨血清sST2和miR-223作为屋尘螨(HDM)诱导的中重度过敏性鼻炎(MSAR)患者接受舌下免疫治疗(SLIT)时疾病活动度和治疗相关变化的潜在生物标志物。本研究纳入54例中重度AR(MSAR)患者和54例健康对照(HC)。检测血清sST2、总IgE、HDM特异性IgE和嗜酸性粒细胞计数。采用实时PCR评估血清miR-223相对表达量。采用总鼻症状评分(TNSS)和视觉模拟量表(VAS)评估临床严重程度。MSAR患者接受SLIT治疗6个月。治疗反应定义为TNSS较基线降低≥30%。MSAR患者血清sST2和miR-223显著高于健康对照(p<0.001)。sST2与HDM特异性IgE和嗜酸性粒细胞计数呈正相关,并在治疗6个月后显著下降(p<0.001)。治疗后sST2在应答者中较低,而基线sST2在组间无显著差异。ROC分析显示sST2(AUC=0.933)和miR-223(AUC≈0.96)对MSAR与HC具有良好区分能力。血清sST2和miR-223显示出作为HDM诱导的MSAR候选生物标志物的良好潜力。治疗后sST2下降提示其可能有助于监测治疗相关变化。需要进一步研究验证这些发现。试验注册:回顾性注册于ClinicalTrials.gov,注册日期为2026年2月25日,标识符(NCT07436208)。注册网址:https://clinicaltrials.gov/study/NCT07436208。

英文摘要

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.