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Respiratory syncytial virus prevents the subsequent development of ovalbumin-induced allergic responses by inhibiting ILC2 via the IL-33/ST2 pathway

    Dandan Wang

    Department of Medical Laboratory, Shengjing Hospital of China Medical University, Shenyang, Liaoning, 110004, PR China

    Department of Immunology, School of Basic Medical Science, China Medical University, Shenyang, 110122, PR China

    ,
    Song Bai

    Department of Immunology, School of Basic Medical Science, China Medical University, Shenyang, 110122, PR China

    ,
    Yulin Cui

    Department of Immunology, School of Basic Medical Science, China Medical University, Shenyang, 110122, PR China

    ,
    Na Zhao

    Department of Immunology, School of Basic Medical Science, China Medical University, Shenyang, 110122, PR China

    ,
    Feifei Qi

    Department of Immunology, School of Basic Medical Science, China Medical University, Shenyang, 110122, PR China

    ,
    Jing Liu

    Department of Immunology, School of Basic Medical Science, China Medical University, Shenyang, 110122, PR China

    ,
    Sheng Zeng

    Department of Immunology, School of Basic Medical Science, China Medical University, Shenyang, 110122, PR China

    ,
    Lei Xu

    Department of Immunology, School of Basic Medical Science, China Medical University, Shenyang, 110122, PR China

    ,
    Haiyan Hu

    Department of Immunology, School of Basic Medical Science, China Medical University, Shenyang, 110122, PR China

    &
    Beixing Liu

    *Author for correspondence: Fax: +86 24 2325 5291;

    E-mail Address: bxliu@cmu.edu.cn

    Department of Immunology, School of Basic Medical Science, China Medical University, Shenyang, 110122, PR China

    Published Online:https://doi.org/10.2217/imt-2018-0059

    Aim: How respiratory syncytial virus (RSV) influences the development of ovalbumin (OVA)-induced asthma remains elusive. As potent T helper (Th)2 cytokine producers, group 2 innate lymphoid cells (ILC2s) are known to serve important functions in the pathogenesis of allergic inflammation. However, how RSV infection affects innate immunity, especially with regard to the function of ILC2s in OVA-induced allergic airway inflammation, is largely unknown. Materials & methods: RSV was used to infect adult BALB/c mice intranasally prior to sensitization and subsequent challenge with OVA. ILC2 frequencies and Th2 cytokine production by ILC2s were assessed by flow cytometry. Cytokine levels were detected both by real-time PCR and ELISA. Results: Previous infection with RSV attenuated airway inflammation and decreased Th2 cytokine production in mice sensitized and challenged with OVA. Furthermore, previous infection with RSV inhibited the influx of ILC2s into the lung, and constrained their Th2 cytokine production. Adoptive transfer of ILC2s increased asthma-associated airway inflammation in mice previously infected with RSV. These results indicate that previous infection with RSV prevents OVA-induced asthma development via inhibition of ILC2s. Previous infection with RSV attenuated IL-33 production in lung tissue and reduced relative ST2L expression in lung ILC2s, meaning that previous infection with RSV may alter ILC2 function via the IL-33/ST2 signaling pathway. Conclusion: These results demonstrate that previous infection with RSV attenuates OVA-induced airway inflammation by inhibiting the recruitment and Th2 cytokine production of ILC2s via the IL-33/ST2 pathway.

    Papers of special note have been highlighted as: • of interest; •• of considerable interest

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