Zhang Liwen, Huang Zhiying, Wang Fei, Xue Mei, Zhang Xiaoyu, Wan Yu, Ma Liang
Department of Pediatrics, The Second People's Hospital of Changzhou, Affiliated Hospital of Nanjing Medical University, Changzhou, Jiangsu, China.
Department of Gastroenterology, The First People's Hospital of Changzhou, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China.
Evid Based Complement Alternat Med. 2023 May 23;2023:2815219. doi: 10.1155/2023/2815219. eCollection 2023.
Respiratory syncytial virus (RSV) is the main pathogen causing acute bronchiolitis, which is common in infants and young children. A previous study revealed the possible involvement of POU class 2 associating factor 1 (POU2AF1) in RSV-triggered acute bronchiolitis. We attempted to clarify the specific action mechanism of POU2AF1 underlying RSV-triggered inflammation.
RT-qPCR measured POU2AF1 levels in RSV-infected children, mice, and airway epithelial cell lines (HBECs). HE staining showed histopathological features in the lung tissue of RSV-infected mice. ELISA examined the contents of proinflammatory cytokines in RSV-infected mice. Western blotting evaluated the protein abundance of proinflammatory cytokines in RSV-infected HBECs and assessed NF-B pathway-associated protein expression in RSV-infected mice and RSV-treated HBECs.
POU2AF1 presented depletion in RSV-infected children, mice, and HBECs. RSV-infected triggered lung injury and inflammatory cell infiltration in the mouse lung tissue, while POU2AF1 overexpression rescued these changes. RSV-infected induced inflammatory impairment in HBECs, whereas POU2AF1 reversed this effect. POU2AF1 suppressed the upregulated NF-B pathway-associated protein expression in mice and HBECs under RSV infection.
POU2AF1 exerts a protective impact on RSV-induced acute bronchiolitis in vitro and in vivo through the NF-B pathway. Our research may provide a novel direction for better therapy of RSV-triggered acute bronchiolitis.
呼吸道合胞病毒（RSV）是引起急性细支气管炎的主要病原体，在婴幼儿中常见。先前的一项研究揭示了POU2类相关因子1（POU2AF1）可能参与RSV引发的急性细支气管炎。我们试图阐明POU2AF1在RSV引发炎症中的具体作用机制。
RT-qPCR检测RSV感染儿童、小鼠和气道上皮细胞系（HBECs）中POU2AF1的水平。HE染色显示RSV感染小鼠肺组织的组织病理学特征。ELISA检测RSV感染小鼠促炎细胞因子的含量。蛋白质印迹法评估RSV感染的HBECs中促炎细胞因子的蛋白丰度，并评估RSV感染小鼠和RSV处理的HBECs中NF-κB通路相关蛋白的表达。
POU2AF1在RSV感染的儿童、小鼠和HBECs中表达降低。RSV感染引发小鼠肺组织的肺损伤和炎性细胞浸润，而POU2AF1过表达可挽救这些变化。RSV感染诱导HBECs发生炎症损伤，而POU2AF1可逆转这种作用。POU2AF1抑制RSV感染小鼠和HBECs中NF-κB通路相关蛋白表达的上调。
POU2AF1通过NF-κB通路在体外和体内对RSV诱导的急性细支气管炎发挥保护作用。我们的研究可能为更好地治疗RSV引发的急性细支气管炎提供新的方向。
