Background/Aim. Bronchiolitis is a common acute lower respiratory tract infectious disease in infants. Respiratory syncytial virus (RSV) infection is one of the main causes. Bronchiolitis can lead to a significant increase in the incidence of asthma in young children, but the mechanism of bronchiolitis transforming into asthma is still unclear. The study was aimed at investigating the role of NF-κB/IL-33/ST2 axis on RSV-induced acute bronchiolitis. Methods. A total of 40 infants diagnosed with acute bronchiolitis infected by RSV, and 20 normal infants were included in this study. BALB/c mice (6-8 weeks old,  g) were used as study models. Enzyme-linked immunosorbent assay (ELISA), quantitative real time PCR, western blot analysis, immunohistochemical staining, and flow cytometry analysis were performed to examine relevant indicators. Results. IL-33 level was significantly elevated, and Th1/Th2 ratio is imbalance after in infants with acute bronchiolitis. In vivo study, we found that NF-κB/IL-33/ST2 axis is mediated the Th2 cytokine levels and BAL cell number induced by RSV. Acute bronchiolitis induced by RSV in a mouse model is attenuated after inhibition of NF-κB/IL-33/ST2 pathway. Moreover, we also confirmed that macrophages are important sources of IL-33 and are regulated by NF-κB pathway in RSV-induced mice. Conclusion. We confirmed that inhibition of NF-κB/IL-33/ST2 axis could attenuate acute bronchiolitis by RSV infected. Our findings not only demonstrate the potential role of IL-33 antibody in attenuating RSV-induced lung damage but also provide a new insight into better prevention of RSV-induced asthma by mediating NF-κB/IL-33/ST2 axis.

中文翻译：

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抑制 NF-κB/IL-33/ST2 轴改善呼吸道合胞病毒诱导的急性毛细支气管炎

背景/目标。细支气管炎是婴儿常见的急性下呼吸道传染病。呼吸道合胞病毒（RSV）感染是主要原因之一。细支气管炎可导致幼儿哮喘发病率显着增加，但细支气管炎转化为哮喘的机制尚不清楚。该研究旨在调查 NF- κ B/IL-33/ST2 轴在 RSV 诱导的急性细支气管炎中的作用。方法。本研究共纳入RSV感染急性毛细支气管炎婴儿40例，正常婴儿20例。BALB/c 小鼠（6-8 周龄， g) 用作研究模型。进行酶联免疫吸附试验（ELISA）、实时定量PCR、蛋白质印迹分析、免疫组织化学染色和流式细胞术分析以检查相关指标。结果。婴儿急性毛细支气管炎后IL-33水平显着升高，Th1/Th2比值失衡。在体内研究中，我们发现 NF- κ B/IL-33/ST2 轴介导了 RSV 诱导的 Th2 细胞因子水平和 BAL 细胞数量。抑制 NF- κ B/IL-33/ST2 通路后，小鼠模型中 RSV 诱导的急性毛细支气管炎得到缓解。此外，我们还证实巨噬细胞是 IL-33 的重要来源，并且在 RSV 诱导的小鼠中受 NF- κ B 通路的调节。结论. 我们证实抑制 NF- κ B/IL-33/ST2 轴可以减轻 RSV 感染引起的急性细支气管炎。我们的研究结果不仅证明了 IL-33 抗体在减轻 RSV 诱导的肺损伤中的潜在作用，而且还为通过介导 NF- κ B/IL-33/ST2 轴更好地预防 RSV 诱导的哮喘提供了新的见解。