Luteolin inhibits respiratory syncytial virus replication by regulating the MiR-155/SOCS1/STAT1 signaling pathway
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RESEARCH
Luteolin inhibits respiratory syncytial virus replication by regulating the MiR‑155/SOCS1/ STAT1 signaling pathway Saisai Wang1, Yiting Ling1, Yuanyuan Yao1, Gang Zheng2 and Wenbin Chen1*
Abstract Background: Respiratory syncytial virus (RSV) is a major cause of acute lower respiratory tract infection in infants, children, immunocompromised adults, and elderly individuals. Currently, there are few therapeutic options available to prevent RSV infection. The present study aimed to investigate the effects of luteolin on RSV replication and the related mechanisms. Material and methods: We pretreated cells and mice with luteolin before infection with RSV, the virus titer, expressions of RSV-F, interferon (IFN)-stimulated genes (ISGs), and production of IFN-α and IFN-β were determined by plaque assay, RT-qPCR, and ELISA, respectively. The activation of Janus kinase (JAK)-signal transducer and activator of transcription 1 (STAT1) signaling pathway was detected by Western blotting and luciferase assay. Proteins which negatively regulate STAT1 were determined by Western blotting. Then cells were transfected with suppressor of cytokine signaling 1 (SOCS1) plasmid and virus replication and ISGs expression were determined. Luciferase reporter assay and Western blotting were performed to detect the relationship between SOCS1 and miR-155. Results: Luteolin inhibited RSV replication, as shown by the decreased viral titer and RSV-F mRNA expression both in vitro and in vivo. The antiviral activity of luteolin was attributed to the enhanced phosphorylation of STAT1, resulting in the increased production of ISGs. Further study showed that SOCS1 was downregulated by luteolin and SOCS1 is a direct target of microRNA-155 (miR-155). Inhibition of miR-155 rescued luteolin-mediated SOCS1 downregulation, whereas upregulation of miR-155 enhanced the inhibitory effect of luteolin. Conclusion: Luteolin inhibits RSV replication by regulating the miR-155/SOCS1/STAT1 signaling pathway. Keywords: Respiratory syncytial virus (RSV), Luteolin, Suppressor of cytokine signaling 1 (SOCS1), microRNA-155 (miR-155), Signal transducer and activator of transcription 1 (STAT1) Background Human respiratory syncytial virus (RSV) is an enveloped, negative-sense, single-strand RNA (ssRNA) virus of the Pneumoviridae family [1]. RSV is the primary cause of respiratory infection in infants and children, resulting *Correspondence: [email protected] 1 Department of Colorectal Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, 79 Qingchun Road, Hangzhou 310003, Zhejiang, People’s Republic of China Full list of author information is available at the end of the article
in pneumonia and bronchiolitis. Moreover, severe RSV infection is related to the development of recurrent wheezing or asthma [2]. In elderly individuals (65 years of age or older), RSV is also an important cause of respiratory infection [3]. Although continuous progress has been made in the development of an RSV vaccine [4], effective treatmen
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