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Blood, 1 November 2003, Vol. 102, No. 9, pp. 3387-3395.
Prepublished online as a Blood First Edition Paper on July 17, 2003; DOI 10.1182/blood-2003-02-0621.
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PHAGOCYTES
Murine neutrophils require 1,3-fucosylation but not PSGL-1 for productive infection with Anaplasma phagocytophilum
Jason A. Carlyon,
Mustafa Akkoyunlu,
Lijun Xia,
Tadayuki Yago,
Tian Wang,
Richard D. Cummings,
Rodger P. McEver, and
Erol Fikrig
From the Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT; Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK; and Department of Biochemistry and Molecular Biology, Oklahoma Center for Medical Glycobiology, University of Oklahoma Health Sciences Center, Oklahoma City, OK.
Anaplasma phagocytophilum causes human granulocytic ehrlichiosis, the second most common tick-borne disease in the United States. Mice are natural reservoirs for this bacterium and man is an inadvertent host. A phagocytophilum's tropism for human neutrophils is linked to neutrophil expression of P-selectin glycoprotein ligand-1 (PSGL-1), as well as sialylated and 1,3-fucosylated glycans. To determine whether A phagocytophilum uses similar molecular features to infect murine neutrophils, we assessed in vitro bacterial binding to neutrophils from and infection burden in wild-type mice; mice lacking 1,3-fucosyltransferases Fuc-TIV and Fuc-TVII; or mice lacking PSGL-1. Binding to Fuc-TIV-/-/Fuc-TVII-/- neutrophils and infection of Fuc-TIV-/-/Fuc-TVII-/- mice were significantly reduced relative to wild-type mice. A phagocytophilum binding to PSGL-1-/- neutrophils was modestly reduced, whereas sialidase treatment significantly decreased binding to both wild-type and PSGL-1-/- neutrophils. A phagocytophilum similarly infected PSGL-1-/- and wild-type mice in vivo. A phagocytophilum induced comparable levels of chemokines from wild-type and PSGL-1-/- neutrophils in vitro, while those induced from Fuc-TIV-/-/Fuc-TVII-/- neutrophils were appreciably reduced. Therefore, A phagocytophilum infection in mice, as in humans, requires sialylation and 1,3-fucosylation of neutrophils. However, murine infection does not require neutrophil PSGL-1 expression, which has important implications for understanding how A phagocytophilum binds and infects neutrophils.

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