Background. Respiratory syncytial virus (RSV) infects infants and children, predisposing them to development of asthma during adulthood. Epithelial neuroendocrine phenotypes may be associated with development of asthma. This study hopes to ascertain if RSV infection promotes epithelial neuroendocrine phenotypes through the NODAL signaling pathway. Methods. The GSE6802 data set was obtained from the GEO database, and the differential genes were analyzed using the language. An in vitro model was constructed with RSV infected human respiratory epithelial cells, and then real-time qPCR and immunofluorescence were used to detect the expression of different epithelial biomarkers and airway neuropeptides. The acute and chronic infection model of RSV infection was established by intranasal injection of RSV into guinea pigs. Immunohistochemistry and Western blot were used to detect the expression of pulmonary neuroendocrine cells markers ENO2 and neuropeptides. Results. The expression levels of ENO2, SP, CGRP, and NODAL/ACTRII were significantly higher in the RSV infection group than those of the control group, which were abrogated by siRNA-NODAL. In vivo, we found that the expression levels of ENO2, SP, and CGRP were significantly higher than that of the control group. Conclusion. RSV promotes epithelial neuroendocrine phenotypes through the NODAL signaling pathway.

中文翻译：

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RSV 通过 NODAL 信号通路促进上皮神经内分泌表型分化

背景。呼吸道合胞病毒 (RSV) 感染婴儿和儿童，使他们在成年期易患哮喘。上皮神经内分泌表型可能与哮喘的发展有关。本研究希望确定 RSV 感染是否通过 NODAL 信号通路促进上皮神经内分泌表型。方法。GSE6802数据集取自GEO数据库，差异基因分析使用语言。用RSV感染的人呼吸道上皮细胞构建体外模型，然后使用实时qPCR和免疫荧光检测不同上皮生物标志物和气道神经肽的表达。通过向豚鼠鼻内注射RSV，建立RSV感染的急慢性感染模型。免疫组化和Western blot检测肺神经内分泌细胞标志物ENO2和神经肽的表达。结果。RSV感染组ENO2、SP、CGRP和NODAL/ACTRII的表达水平显着高于对照组，而对照组则被siRNA-NODAL消除。在体内，我们发现ENO2、SP和CGRP的表达水平显着高于对照组。结论。RSV 通过 NODAL 信号通路促进上皮神经内分泌表型。