IFN-τ Plays an Anti-Inflammatory Role in Staphylococcus aureus-Induced Endometritis in Mice Through the Suppression of NF-κB Pathway and MMP9 Expression
Interferon-tau (IFN-τ) is a type I interferon and considered as a pregnancy recognition signal in ruminants. Our previous reports have confirmed that IFN-τ has a potential anti-inflammatory effect in macrophage. However, the anti-inflammatory effect of IFN-τ on endometritis has never been reported....
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Veröffentlicht in: | Journal of interferon & cytokine research 2017-02, Vol.37 (2), p.81-89 |
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Sprache: | eng |
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Zusammenfassung: | Interferon-tau (IFN-τ) is a type I interferon and considered as a pregnancy recognition signal in ruminants. Our previous reports have confirmed that IFN-τ has a potential anti-inflammatory effect in macrophage. However, the anti-inflammatory effect of IFN-τ on endometritis has never been reported. Thus, the aim of this study was to investigate the effects of IFN-τ in a mouse model of Staphylococcus aureus-induced endometritis. The histopathological and myeloperoxidase activity results showed that IFN-τ could protect the uterus from S. aureus damage. Enzyme-linked immunosorbent assay and quantitative real-time polymerase chain reaction results revealed that IFN-τ inhibited TNF-α, IL-1β, and IL-6 production. TLR2, involved in the S. aureus infection, was downregulated by IFN-τ and directly activated nuclear transcription factor kappa-B (NF-κB) pathway. Then, we measured the phosphorylation of IκBα and NF-κB p65 by Western blotting. Western blotting results indicated that IFN-τ inhibited the phosphorylation of IκBα and NF-κB p65 in the S. aureus-induced endometritis. Matrix metalloproteinase (MMP)9, which has been reported to be regulated by NF-κB, was also suppressed by IFN-τ, but its inhibitors, tissue inhibitor of metalloproteinases1 level, increased. All of these findings suggested that IFN-τ plays an anti-inflammatory role in S. aureus-induced endometritis by suppressing NF-κB pathway and MMP9 expression. |
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ISSN: | 1079-9907 1557-7465 |
DOI: | 10.1089/jir.2016.0058 |