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Infection and Immunity, October 2000, p. 5496-5501, Vol. 68, No. 10
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Production of Borreliacidal Antibody to Outer Surface Protein A In Vitro and Modulation by Interleukin-4

Erik L. Munson,1,2 Brian K. Du Chateau,1,3,dagger Dean A. Jobe,4 Steven D. Lovrich,4 Steven M. Callister,4,5 and Ronald F. Schell1,2,3,*

Wisconsin State Laboratory of Hygiene1 and Departments of Medical Microbiology and Immunology2 and Bacteriology,3 University of Wisconsin, Madison, Wisconsin 53706, and Microbiology Research Laboratory4 and Department of Infectious Diseases,5 Gundersen Lutheran Medical Center, La Crosse, Wisconsin 54601

Received 21 March 2000/Returned for modification 12 May 2000/Accepted 30 June 2000

Borreliacidal antibody production is one of several parameters for establishing the effectiveness of Borrelia burgdorferi vaccines. The production of borreliacidal antibody was studied in vitro by culturing immune lymph node cells with macrophages and B. burgdorferi. We showed that borreliacidal antibody, directed primarily against outer surface protein A (OspA), was readily produced by lymph node cells obtained from C3H/HeJ mice vaccinated with formalin-inactivated B. burgdorferi in aluminum hydroxide, but not recombinant OspA. Anti-OspA borreliacidal antibody was detected in supernatants of cultures of lymph node cells obtained on day 7 after vaccination, peaked on day 17, and rapidly declined. The borreliacidal activity was attributable to immunoglobulin G1 (IgG1), IgG2a, and IgG2b antibodies. When lymph node cells were treated with interleukin-4 (IL-4), production of borreliacidal antibody was inhibited but was unaffected by treatment with anti-IL-4 antibodies. These results suggest that other cytokines, but not IL-4, are mainly responsible for production of the secondary borreliacidal antibody response.

* Corresponding author. Mailing address: Wisconsin State Laboratory of Hygiene, University of Wisconsin, 465 Henry Mall, Madison, WI 53706. Phone: (608) 262-3634. Fax: (608) 265-3451. E-mail: RFSchell{at}Facstaff.wisc.edu.

dagger Present address: Path Lab, Incorporated, Portsmouth, NH 03801.

Infection and Immunity, October 2000, p. 5496-5501, Vol. 68, No. 10
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Munson, E. L., Nardelli, D. T., Luk, K. H. K., Remington, M. C., Callister, S. M., Schell, R. F. (2006). Interleukin-6 Promotes Anti-OspA Borreliacidal Antibody Production In Vitro. CVI 13: 19-25 [Abstract] [Full Text]  
  • Munson, E. L., DeCoster, D. J., Nardelli, D. T., England, D. M., Callister, S. M., Schell, R. F. (2004). Neutralization of Gamma Interferon Augments Borreliacidal Antibody Production and Severe Destructive Lyme Arthritis in C3H/HeJ Mice. CVI 11: 35-41 [Abstract] [Full Text]  
  • Munson, E. L., Du Chateau, B. K., Jensen, J. R., Callister, S. M., DeCoster, D. J., Schell, R. F. (2002). Gamma Interferon Inhibits Production of Anti-OspA Borreliacidal Antibody In Vitro. CVI 9: 1095-1101 [Abstract] [Full Text]  
  • Remington, M. C., Munson, E. L., Callister, S. M., Molitor, M. L., Christopherson, J. A., DeCoster, D. J., Lovrich, S. D., Schell, R. F. (2001). Interleukin-6 Enhances Production of Anti-OspC Immunoglobulin G2b Borreliacidal Antibody. Infect. Immun. 69: 4268-4275 [Abstract] [Full Text]  


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