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Infection and Immunity, December 2008, p. 5500-5507, Vol. 76, No. 12
0019-9567/08/$08.00+0     doi:10.1128/IAI.00808-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Adenoviral Delivery of Interleukin-10 Fails To Attenuate Experimental Lyme Disease{triangledown}

Charles R. Brown,1,2* Annie Y.-C. Lai,1 Steven T. Callen,1 Victoria A. Blaho,1 Jennifer M. Hughes,1 and William J. Mitchell1

Departments of Veterinary Pathobiology,1 Molecular Microbiology and Immunology, University of Missouri, Columbia, Missouri 652112

Received 30 June 2008/ Returned for modification 22 July 2008/ Accepted 24 September 2008

Production of interleukin-10 (IL-10) by C57BL/6 mice following infection with Borrelia burgdorferi has been proposed as a mechanism whereby resistance to the development of experimental Lyme arthritis is maintained. In the current study, we sought to determine the role of IL-10 during infection of arthritis- and carditis-susceptible C3H mice. Infection of C3H IL-10–/– mice led to increased joint swelling and arthritis severity scores over those of wild-type C3H mice. Measurement of B. burgdorferi numbers in joints or disseminated tissues indicated a more efficient clearance of spirochetes in the absence of IL-10, similar to that reported in C57BL/6 IL-10–/– mice. However, in contrast to previous in vitro work, infection of C3H IL-10–/– mice led to decreased in vivo expression of the cytokines KC, IL-1β, IL-4, and IL-12p70 in the infected joints. Finally, adenoviral expression of IL-10 in the infected joints of C3H mice was unable to modulate the development of severe Lyme arthritis and had no effect on spirochete clearance or Borrelia-specific antibody production. Development of Lyme carditis appeared to be independent of modulation by IL-10. These results suggest that IL-10 limits the development of joint inflammation in both arthritis-resistant and -susceptible mouse strains infected with B. burgdorferi and that increased IL-10 production cannot rescue genetic susceptibility to development of pathology in this model.

* Corresponding author. Mailing address: Department of Veterinary Pathobiology, 315 Connaway Hall, University of Missouri, Columbia, MO 65211. Phone: (573) 882-1628. Fax: (523) 884-5414. E-mail: Brownchar{at}missouri.edu

{triangledown} Published ahead of print on 29 September 2008.

Editor: R. P. Morrison

Infection and Immunity, December 2008, p. 5500-5507, Vol. 76, No. 12
0019-9567/08/$08.00+0     doi:10.1128/IAI.00808-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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