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Infection and Immunity, August 2003, p. 4432-4440, Vol. 71, No. 8
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.8.4432-4440.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Effect of Complement Component C3 Deficiency on Experimental Lyme Borreliosis in Mice

Matthew B. Lawrenz,1 R. Mark Wooten,2 James F. Zachary,3 Scott M. Drouin,4 Janis J. Weis,5 Rick A. Wetsel,4 and Steven J. Norris1*

Program in Microbiology and Molecular Genetics and Department of Pathology and Laboratory Medicine, Graduate School of Biomedical Sciences,1 Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas—Houston Health Science Center, Houston, Texas,4 Department of Microbiology and Immunology, Medical College of Ohio, Toledo, Ohio,2 Department of Veterinary Pathobiology, College of Veterinary Medicine, University of Illinois, Urbana, Illinois,3 Department of Pathology, University of Utah, Salt Lake City, Utah5

Received 3 February 2003/ Returned for modification 25 March 2003/ Accepted 2 May 2003

Mice deficient in complement component C3 (C3-/-) and syngeneic C57BL/6 control mice were challenged with Borrelia burgdorferi to determine the role of complement in immune clearance and joint histopathology during experimental Lyme borreliosis. Tibiotarsal joint, ear, and heart tissues were monitored for spirochete numbers at 2, 4, 8, and 12 weeks postinoculation with 105 B. burgdorferi B31 clone 5A4 by using quantitative real-time PCR. The spirochete load in joint and ear tissue remained higher in the C3-/- mice than in the wild-type counterparts throughout the 12-week study, whereas the numbers in heart tissue of both groups of mice decreased substantially at 8 to 12 weeks postinfection. Histopathology scores for joint tissue were generally higher in the C3-/- mice compared to C57BL/6 controls at 2 and 4 weeks postinfection, which may reflect the presence of higher numbers of bacteria in the joints at these early time points. Levels of anti-B. burgdorferi immunoglobulin G tended to be reduced in the C3-/- mice compared to control mice. Furthermore, a 5.5-fold-lower number of the complement-sensitive Borrelia garinii was needed to infect C3-/- mice compared to C57BL/6 mice, indicating that its sensitivity to complement is one barrier to infection of the mouse model by B. garinii. These results indicate that the complement system may be important in controlling the early dissemination and progression of B. burgdorferi infection.

* Corresponding author. Mailing address: Department of Pathology and Laboratory Medicine, University of Texas Medical School at Houston, P.O. Box 20708, Houston, TX 77225-0708. Phone: (713) 500-5338. Fax: (713) 500-0738. E-mail: Steven.J.Norris{at}uth.tmc.edu.

Editor: D. L. Burns

Infection and Immunity, August 2003, p. 4432-4440, Vol. 71, No. 8
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.8.4432-4440.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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