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Infection and Immunity, December 2003, p. 6728-6733, Vol. 71, No. 12
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.12.6728-6733.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Divergent Interactions of Ehrlichia chaffeensis- and Anaplasma phagocytophilum-Infected Leukocytes with Endothelial Cell Barriers

Jinho Park,1 Kyoung-Seong Choi,1 Dennis J. Grab,2 and J. Stephen Dumler1*

Division of Medical Microbiology, Department of Pathology,1 Division of Infectious Diseases, Department of Pediatrics, The Johns Hopkins University School of Medicine, Baltimore, Maryland2

Received 27 May 2003/ Returned for modification 26 July 2003/ Accepted 20 August 2003

Human anaplasmosis (formerly human granulocytic ehrlichiosis) and human monocytic ehrlichiosis (HME) are emerging tick-borne infections caused by obligate intracellular bacteria in the family Anaplasmataceae. Clinical findings include fever, headache, myalgia, leukopenia, thrombocytopenia, and hepatic inflammatory injury. Whereas Ehrlichia chaffeensis (HME) often causes meningoencephalitis, this is rare with Anaplasma phagocytophilum infection. The abilities of infected primary host monocytes and neutrophils and of infected HL-60 cells to cross human umbilical vein endothelial cell-derived EA.hy926 cell barriers and human brain microvascular cells (BMEC), a human blood-brain barrier model, were studied. Uninfected monocyte/macrophages crossed endothelial cell barriers six times more efficiently than neutrophils. More E. chaffeensis-infected monocytes transmigrated than uninfected monocytes, whereas A. phagocytophilum suppressed neutrophil transmigration. Differences were not due to barrier dysfunction, as transendothelial cell resistivities were the same for uninfected cell controls. Similar results were obtained for HL-60 cells used as hosts for E. chaffeensis and A. phagocytophilum. Differential transmigration of E. chaffeensis- and A. phagocytophilum-infected leukocytes and HL-60 cells confirmed a role for the pathogen in modifying cell migratory capacity. These results support the hypothesis that Anaplasmataceae intracellular infections lead to unique pathogen-specific host cell functional alterations that are likely important for pathogen survival, pathogenesis, and disease induction.

* 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) 955-8654. Fax: (443) 287-3665. E-mail: sdumler{at}jhmi.edu.

Editor: W. A. Petri, Jr.

Infection and Immunity, December 2003, p. 6728-6733, Vol. 71, No. 12
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.12.6728-6733.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Grab, D. J., Perides, G., Dumler, J. S., Kim, K. J., Park, J., Kim, Y. V., Nikolskaia, O., Choi, K. S., Stins, M. F., Kim, K. S. (2005). Borrelia burgdorferi, Host-Derived Proteases, and the Blood-Brain Barrier. Infect. Immun. 73: 1014-1022 [Abstract] [Full Text]  
  • Garyu, J. W. A., Choi, K.-s., Grab, D. J., Dumler, J. S. (2005). Defective Phagocytosis in Anaplasma phagocytophilum- Infected Neutrophils. Infect. Immun. 73: 1187-1190 [Abstract] [Full Text]  
  • Choi, K.-s., Grab, D. J., Dumler, J. S. (2004). Anaplasma phagocytophilum Infection Induces Protracted Neutrophil Degranulation. Infect. Immun. 72: 3680-3683 [Abstract] [Full Text]  


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