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Clinical and Diagnostic Laboratory Immunology, September 2004, p. 963-968, Vol. 11, No. 5
1071-412X/04/$08.00+0     DOI: 10.1128/CDLI.11.5.963-968.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

CXCR2 Blockade Influences Anaplasma phagocytophilum Propagation but Not Histopathology in the Mouse Model of Human Granulocytic Anaplasmosis

Diana G. Scorpio,1 Mustafa Akkoyunlu,2,{dagger} Erol Fikrig,2 and J. Stephen Dumler3*

Department of Comparative Medicine,1 Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland,3 Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut2

Received 19 April 2004/ Returned for modification 14 May 2004/ Accepted 8 June 2004

Anaplasma phagocytophilum is an obligate intracellular bacterium that infects neutrophils and causes human granulocytic anaplasmosis. Infection induces neutrophil secretion of interleukin-8 or murine homologs and perpetuates infection by recruiting susceptible neutrophils. We hypothesized that antibody blockade of CXCR2 would decrease A. phagocytophilum tissue load by interrupting neutrophil recruitment but would not influence murine hepatic pathology. C3H-scid mice were treated with CXCR2 antiserum or control prior to or on day 14 after infection. Quantitative PCR and immunohistochemistry for A. phagocytophilum were performed and severity of liver histopathology was ranked. Control mice had more infected cells in tissues than the anti-CXCR2-treated group. The histopathological rank was not different between treated and control animals. Infected cells of control mice clustered in tissue more than in treated mice. The results support the hypothesis of bacterial propagation through chemokine induction and confirm that tissue injury is unrelated to A. phagocytophilum tissue load.

* Corresponding author. Mailing address: Department of Pathology, The Johns Hopkins University School of Medicine, 720 Rutland Ave., Baltimore, MD 21205. Phone: (410) 955-8654. Fax: (443) 287-3665. E-mail: sdumler{at}jhmi.edu.

{dagger} Present address: Food and Drug Administration, Center for Biologics Evaluation and Research, Rockville, MD 20852.

Clinical and Diagnostic Laboratory Immunology, September 2004, p. 963-968, Vol. 11, No. 5
1071-412X/04/$08.00+0     DOI: 10.1128/CDLI.11.5.963-968.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Johns, J. L., MacNamara, K. C., Walker, N. J., Winslow, G. M., Borjesson, D. L. (2009). Infection with Anaplasma phagocytophilum Induces Multilineage Alterations in Hematopoietic Progenitor Cells and Peripheral Blood Cells. Infect. Immun. 77: 4070-4080 [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]  


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