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    The role of type I interferons (IFNs) in the regulation of chicken macrophage inflammatory response to bacterial challenge (2018)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Garrido, Damien
    Alber, Andreas
    Kut, Emmanuel
    Chanteloup, Nathalie K
    Lion, Adrien
    Trotereau, Angélina
    Dupont, Joëlle
    Tedin, Karsten (WE 7)
    Kaspers, Bernd
    Vervelde, Lonneke
    Trapp, Sascha
    Schouler, Catherine
    Guabiraba, Rodrigo
    Quelle
    Developmental and comparative immunology
    Bandzählung: 86
    Seiten: 156 – 170
    ISSN: 0145-305x
    Sprache
    Englisch
    Verweise
    DOI: 10.1016/j.dci.2018.04.025
    Pubmed: 29729283
    Kontakt
    Institut für Mikrobiologie und Tierseuchen

    Robert-von-Ostertag-Str. 7-13
    14163 Berlin
    +49 30 838 51843 / 66949
    mikrobiologie@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    Mammalian type I interferons (IFNα/β) are known to modulate inflammatory processes in addition to their antiviral properties. Indeed, virus-induced type I interferons regulate the mammalian phagocyte immune response to bacteria during superinfections. However, it remains unresolved whether type I IFNs similarly impact the chicken macrophage immune response. We first evidenced that IFNα and IFNβ act differently in terms of gene expression stimulation and activation of intracellular signaling pathways in chicken macrophages. Next, we showed that priming of chicken macrophages with IFNα increased bacteria uptake, boosted bacterial-induced ROS/NO production and led to an increased transcriptional expression or production of NOS2/NO, IL1B/IL-1β and notably IFNB/IFNβ. Neutralization of IFNβ during bacterial challenge limited IFNα-induced augmentation of the pro-inflammatory response. In conclusion, we demonstrated that type I IFNs differently regulate chicken macrophage functions and drive a pro-inflammatory response to bacterial challenge. These findings shed light on the diverse functions of type I IFNs in chicken macrophages.