期刊
BLOOD
卷 102, 期 9, 页码 3387-3395出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2003-02-0621
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- NHLBI NIH HHS [HL 65631] Funding Source: Medline
- NIAID NIH HHS [AI041440, AI48075, AI10554] Funding Source: Medline
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 alpha1,3-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 alpha1,3-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 alpha1,3-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. (C) 2003 by The American Society of Hematology.
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