Defective phagocytosis in Anaplasma phagocytophilum-infected neutrophils.

Anaplasma phagocytophilum infection induces functional neutrophil changes. Using both Candida albicans and fluorescent-aggregate phagocytosis assays, we examined whether neutrophil and dimethyl sulfoxide-differentiated HL-60 cell infection impairs internalization. A. phagocytophilum infection significantly decreased phagocytosis compared to that of controls (P < 0.05). This further impairment of neutrophil function may promote opportunistic infections and exacerbate disease.

Anaplasma phagocytophilum infection reduces expression of phagocytosis-related receptors on neutrophils.

Anaplasma phagocytophilum is a tick-transmitted obligate intracellular bacterium of neutrophils that causes human granulocytic anaplasmosis. Previous data confirm that in vitro infection by A. phagocytophilum modifies neutrophil functions, including a 50% or greater reduction in phagocytosis and shedding of neutrophil cell surface adhesion molecule receptors. If these receptors are downregulated or shed from the surface of neutrophils with A. phagocytophilum infection, it may prevent neutrophils from effective phagocytosis. We hypothesized that diminished phagocytosis in neutrophils is partly associated with the loss of surface phagocytic receptors. To address this, we assayed the expression of these receptors after 24 h of A. phagocytophilum infection in human neutrophils.