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

Infection and immunity (2009-10-28)
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
ABSTRACT

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-gamma)-deficient mice suggested a major role of IFN-gamma in the control of A. phagocytophilum. Here we investigated whether infection of human PMN with A. phagocytophilum impairs IFN-gamma signaling thus facilitating intracellular survival of the bacterium. The secretion of the IFN-gamma-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-gamma receptor alpha-chain CD119, diminished the IFN-gamma-induced phosphorylation of STAT1, and enhanced the expression of SOCS1 and SOCS3 in PMN. Since IFN-gamma activates various antibacterial effector mechanisms of PMN, the impaired IFN-gamma signaling in infected cells likely contributes to the survival of A. phagocytophilum inside PMN and to HGA disease development.

MATERIALS
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Product Description

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