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Infection and Immunity, August 2003, p. 4586-4594, Vol. 71, No. 8
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.8.4586-4594.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Diminished Adhesion of Anaplasma phagocytophilum-Infected Neutrophils to Endothelial Cells Is Associated with Reduced Expression of Leukocyte Surface Selectin

Kyoung-Seong Choi, Justin Garyu, Jinho Park, and J. Stephen Dumler*

Division of Medical Microbiology, Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205

Received 10 March 2003/ Returned for modification 30 April 2003/ Accepted 15 May 2003

Anaplasma phagocytophilum propagates within neutrophils and causes a disease marked by inflammatory tissue injury or complicated by opportunistic infections. We hypothesized that infection with A. phagocytophilum modifies the binding of neutrophils to endothelial cells and the expression of neutrophil adhesion molecules and studied these changes in vitro. Infected dimethyl sulfoxide-differentiated HL-60 cells and neutrophils showed reduced binding to cultured brain and systemic endothelial cells and lost expression of P-selectin glycoprotein ligand 1 (PSGL-1, CD162) and L-selectin (CD62L) (to 33 and 5% of control values, respectively), at a time when the levels of ß2 integrin and immunoglobulin superfamily adhesion molecules and activation markers Mac-1 and intercellular adhesion molecule 1 increased (5 to 10 times that of the control). The loss of CD162 and CD62L expression was inhibited by EDTA, which suggests that neutrophil activation and sheddase cleavage occurred. The loss of selectin expression and the retained viability of the neutrophils persisted for at least 18 h with A. phagocytophilum infection, whereas Escherichia coli and Staphylococcus aureus rapidly killed neutrophils. The adhesion defect might increase the numbers of infected cells and their persistence in the blood prior to tick bites. However, decreased CD162 expression and poor endothelial cell binding may partly explain impaired host defenses, while simultaneous neutrophil activation may aggravate inflammation. These observations may help us to understand the modified biological responses, host inflammation, and immune response that occur with A. phagocytophilum infections.

* Corresponding author. Mailing address: Division of Medical Microbiology, Department of Pathology, The Johns Hopkins University School of Medicine, Ross Research Building, Room 624, 720 Rutland Ave., Baltimore, MD 21205. Phone: (410) 614-2864. Fax: (443) 287-3665. E-mail: sdumler{at}jhmi.edu.

Editor: W. A. Petri, Jr.

Infection and Immunity, August 2003, p. 4586-4594, Vol. 71, No. 8
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.8.4586-4594.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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