Abstract
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 R 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.
Highlights
Respiratory syncytial virus (RSV) is an enveloped RNA virus with a single-stranded negative chain genome
Using bioinformatics to analyze RSV-infected bronchial epithelial cells (BECs), we found that RSV infection can promote the expression levels of pulmonary neuroendocrine cells (PNECs) marker enolase-2 (ENO2) and NODAL/ACTRII in BECs
Focused on the analysis of different epithelial cell markers, and the results showed that the expression of PNECs markers (ENO2) increased after RSV infection, while there were no significant difference in basal cell markers CD44, ciliated cells markers cadherin 1 (CDH1), goblet cell markers mucin 5 AC (MUC5A), and alveolar epithelial type I (AECI) cell markers aquaporin 1 (AQP1) (Figure 1(c))
Summary
Respiratory syncytial virus (RSV) is an enveloped RNA virus with a single-stranded negative chain genome. The PNECs contain a variety of active amines and peptides, such as 5-hydroxytryptamine, calcitonin, calcitonin gene-related peptide (CGRP), and enkephalin [4] These secretions may be involved in regulating the contraction of airway vascular smooth muscle through paracrine action or blood circulation. Respiratory syncytial virus (RSV) infects infants and children, predisposing them to development of asthma during adulthood. This study hopes to ascertain if RSV infection promotes epithelial neuroendocrine phenotypes through the NODAL signaling pathway. An in vitro model was constructed with RSV infected human respiratory epithelial cells, and real-time qPCR and immunofluorescence were used to detect the expression of different epithelial biomarkers and airway neuropeptides. 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. RSV promotes epithelial neuroendocrine phenotypes through the NODAL signaling pathway
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