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Infection and Immunity, September 2004, p. 4956-4965, Vol. 72, No. 9
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.9.4956-4965.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Treatment of Mice with the Neutrophil-Depleting Antibody RB6-8C5 Results in Early Development of Experimental Lyme Arthritis via the Recruitment of Gr-1– Polymorphonuclear Leukocyte-Like Cells

Charles R. Brown,1,2* Victoria A. Blaho,1 and Christie M. Loiacono2

Departments of Molecular Microbiology and Immunology,1 Veterinary Pathobiology, University of Missouri, Columbia, Missouri2

Received 4 February 2004/ Returned for modification 2 March 2004/ Accepted 31 May 2004

Recently, we demonstrated that blocking the entry of neutrophils into Borrelia burgdorferi-infected joints in mice deficient in the chemokine receptor CXCR2 prevented the development of experimental Lyme arthritis. Neutrophils were marginalized in blood vessels at the site of infection but could not enter the joint tissue. In the present study, we treated both genetically arthritis-resistant DBA/2J (DBA) and arthritis-susceptible C3H/HeJ (C3H) mice with the neutrophil-depleting monoclonal antibody RB6-8C5 (RB6) to determine the effect on arthritis development. Surprisingly, both DBA and C3H mice treated with RB6 developed arthritis at 1 week postinfection, approximately 1 week earlier than the control-treated C3H mice. The early development of arthritis in the RB6-treated mice was accompanied by an influx into the joints of cells with ring-shaped polymorphonuclear leukocyte (PMN) cell morphology that were negative for the Gr-1 neutrophil maturation marker. RB6 treatment of mice also resulted in increased numbers of B. burgdorferi cells in the joints at 7 days postinfection and earlier expression of the chemokines KC and monocyte chemoattractant protein 1 in the joints compared to control-treated animals. Together, these results suggest that recruitment of neutrophils or PMN-like cells into an infected joint is a key requirement for Lyme arthritis development and that altered recruitment of these cells into the joints of arthritis-resistant mice can exacerbate the development of pathology.

* Corresponding author: Mailing address: Veterinary Pathobiology, 315 Connaway Hall, University of Missouri, Columbia, MO 65211. Phone: (573) 882-1628. Fax: (573) 884-5414. E-mail: BrownChar{at}missouri.edu.

Editor: J. F. Urban, Jr.

Infection and Immunity, September 2004, p. 4956-4965, Vol. 72, No. 9
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.9.4956-4965.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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