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<p>Influenza A virus (IAV) infection typically induces both innate and adaptive immune mechanisms. IL-33, an “alarmin” cytokine with pro-inflammatory effects, may have roles in IAV infection. IL-33 can be upregulated by the gp130 cytokine Oncostatin M (OSM), which induces Th2-skewed inflammation (eosinophils, Arg1 + Macrophages, IL-33, IL-4, eotaxin-2) in mouse lungs. We here examined both OSM and IL-33 regulation by the IAV-H1N1/PR8 strain. Female C57BL/6 mice infected intranasally with H1N1/PR8 showed time-dependent elevation of OSM expression but a reduction in lung IL-33 protein and mRNA. Since this suggested active suppression of IL-33 by H1N1/PR8, we assessed H1N1/PR8 superinfection in mice with established Th2-skewed inflammation induced by Adenoviral vector overexpressing OSM administered 7 days prior. H1N1/PR8 markedly reduced eosinophil and Arg1 + macrophage accumulation, IL-33, IL-4, and eotaxin-2 expression 5-days post infection. IFNγ partially inhibited OSM-induced IL-33 protein in mouse lung epithelial (C10) cells in vitro, and both basal and OSM-induced IL-33 expression were markedly suppressed by direct H1N1/PR8 infection of C10 cells, whereas TIMP-1 or OSMRβ were not. Collectively, IL-33 was selectively suppressed by H1N1/PR8 infection in part by direct effects of virus on IL-33-expressing epithelial cells. Thus, although influenza infection induces OSM, IAV also selectively suppresses IL-33 and IL-33-mediated downstream Th2-skewed inflammation.</p>

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Influenza A/PR8 virus infection in mice suppresses basal and Oncostatin M-induced IL-33 expression in vivo and in vitro

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月23日

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  • Leila Somani-Davis,
  • Anisha Dubey,
  • Fernando Botelho,
  • Lily Buder,
  • Kyle MacDonald,
  • Matthew Miller,
  • Carl D. Richards

摘要

Influenza A virus (IAV) infection typically induces both innate and adaptive immune mechanisms. IL-33, an “alarmin” cytokine with pro-inflammatory effects, may have roles in IAV infection. IL-33 can be upregulated by the gp130 cytokine Oncostatin M (OSM), which induces Th2-skewed inflammation (eosinophils, Arg1 + Macrophages, IL-33, IL-4, eotaxin-2) in mouse lungs. We here examined both OSM and IL-33 regulation by the IAV-H1N1/PR8 strain. Female C57BL/6 mice infected intranasally with H1N1/PR8 showed time-dependent elevation of OSM expression but a reduction in lung IL-33 protein and mRNA. Since this suggested active suppression of IL-33 by H1N1/PR8, we assessed H1N1/PR8 superinfection in mice with established Th2-skewed inflammation induced by Adenoviral vector overexpressing OSM administered 7 days prior. H1N1/PR8 markedly reduced eosinophil and Arg1 + macrophage accumulation, IL-33, IL-4, and eotaxin-2 expression 5-days post infection. IFNγ partially inhibited OSM-induced IL-33 protein in mouse lung epithelial (C10) cells in vitro, and both basal and OSM-induced IL-33 expression were markedly suppressed by direct H1N1/PR8 infection of C10 cells, whereas TIMP-1 or OSMRβ were not. Collectively, IL-33 was selectively suppressed by H1N1/PR8 infection in part by direct effects of virus on IL-33-expressing epithelial cells. Thus, although influenza infection induces OSM, IAV also selectively suppresses IL-33 and IL-33-mediated downstream Th2-skewed inflammation.