Long non-coding RNA cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) in various diseases has been verified. However, the underlying mechanism of CDKN2B-AS1 contributes to the development of allergic rhinitis (AR) remains unknown. To evaluate the impact of CDKN2B-AS1 on AR, BALB/c mice were sensitized by intraperitoneal injection of normal saline containing ovalbumin (OVA) and calmogastrin to establish an AR model. Nasal rubbing and sneezing were documented after the final OVA treatment. The concentrations of IgE, IgG1, and inflammatory elements were quantified using ELISA. Hematoxylin and eosin (H&E) staining and immunofluorescence were used to assess histopathological variations and tryptase expression, respectively. StarBase, TargetScan and luciferase reporter assays were applied to predict and confirm the interactions among CDKN2B-AS1, miR-98-5p, and SOCS1. CDKN2B-AS1, miR-98-5p, and SOCS1 levels were assessed by quantitative real-time PCR (qRT-PCR) or western blotting. Our results revealed that CDKN2B-AS1 was obviously over-expressed in the nasal mucosa of AR patients and AR mice. Down-regulation of CDKN2B-AS1 significantly decreased nasal rubbing and sneezing frequencies, IgE and IgG1 concentrations, and cytokine levels. Furthermore, down-regulation of CDKN2B-AS1 also relieved the pathological changes in the nasal mucosa, and the infiltration of eosinophils and mast cells. Importantly, these results were reversed by the miR-98-5p inhibitor, whereas miR-98-5p directly targeted CDKN2B-AS1, and miR-98-5p negatively regulated SOCS1 level. Our findings demonstrate that down-regulation of CDKN2B-AS1 improves allergic inflammation and symptoms in a murine model of AR through the miR-98-5p/SOCS1 axis, which provides new insights into the latent functions of CDKN2B-AS1 in AR treatment.

长非编码RNA细胞周期蛋白依赖性激酶抑制剂2B反义RNA 1 (CDKN2B-AS1)在多种疾病中已得到验证。然而，CDKN2B-AS1 导致过敏性鼻炎 (AR) 发展的潜在机制仍不清楚。为了评价CDKN2B-AS1对AR的影响，通过腹腔注射含卵清蛋白（OVA）和钙胃泌素的生理盐水致敏BALB/c小鼠建立AR模型。最终 OVA 治疗后记录了擦鼻和打喷嚏的情况。使用 ELISA 对 IgE、IgG1 和炎症成分的浓度进行定量。苏木精和伊红（H＆E）染色和免疫荧光分别用于评估组织病理学变化和类胰蛋白酶表达。应用 StarBase、TargetScan 和荧光素酶报告基因检测来预测和确认 CDKN2B-AS1、miR-98-5p 和 SOCS1 之间的相互作用。通过定量实时 PCR (qRT-PCR) 或蛋白质印迹评估 CDKN2B-AS1、miR-98-5p 和 SOCS1 水平。我们的结果显示CDKN2B-AS1在AR患者和AR小鼠的鼻粘膜中明显过度表达。CDKN2B-AS1 的下调显着降低了擦鼻和打喷嚏的频率、IgE 和 IgG1 浓度以及细胞因子水平。此外，CDKN2B-AS1的下调也减轻了鼻粘膜的病理变化以及嗜酸性粒细胞和肥大细胞的浸润。重要的是，这些结果被 miR-98-5p 抑制剂逆转，而 miR-98-5p 直接靶向 CDKN2B-AS1，并且 miR-98-5p 负向调节 SOCS1 水平。我们的研究结果表明，CDKN2B-AS1 的下调通过 miR-98-5p/SOCS1 轴改善 AR 小鼠模型中的过敏性炎症和症状，这为 CDKN2B-AS1 在 AR 治疗中的潜在功能提供了新的见解。