Impairment of gamma interferon signaling in human neutrophils infected with Anaplasma phagocytophilum

Uta Bussmeyer, Arup Sarkar, Kirsten Broszat, Tanja Lüdemann, Sonja Möller, Ger Van Zandbergen, Christian Bogdan, Martina Behnen, J. Stephen Dumler, Friederike D. Von Loewenich, Werner Solbach, Tamás Laskay*

*Corresponding author for this work
    17 Citations (Scopus)


    Anaplasma phagocytophilum, the causative agent of tick-borne human granulocytic anaplasmosis (HGA), is an intracellular bacterium which survives and multiplies inside polymorphonuclear neutrophil granulocytes (PMN). Increased bacterial burden in gamma interferon (IFN-γ)-deficient mice suggested a major role of IFN-γ in the control of A. phagocytophilum. Here we investigated whether infection of human PMN with A. phagocytophilum impairs IFN-γ signaling thus facilitating intracellular survival of the bacterium. The secretion of the IFN-γ-inducible chemokines IP-10/CXCL10 and MIG/CXCL9 was markedly inhibited in infected neutrophils. Molecular analyses revealed that, compared to uninfected PMN, A. phagocytophilum decreased the expression of the IFN-γ receptor α-chain CD119, diminished the IFN-γ-induced phosphorylation of STAT1, and enhanced the expression of SOCS1 and SOCS3 in PMN. Since IFN-γ activates various antibacterial effector mechanisms of PMN, the impaired IFN-γ signaling in infected cells likely contributes to the survival of A. phagocytophilum inside PMN and to HGA disease development.

    Original languageEnglish
    JournalInfection and Immunity
    Issue number1
    Pages (from-to)358-363
    Number of pages6
    Publication statusPublished - 01.01.2010

    Research Areas and Centers

    • Academic Focus: Center for Infection and Inflammation Research (ZIEL)


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