Previous Article | Next Article ![]()
Infection and Immunity, October 1999, p. 5142-5150, Vol. 67, No. 10
Division of Cell Biology and Immunology,
Department of Pathology, University of Utah School of Medicine,
Salt Lake City, Utah 84132,1 and
Department of Veterinary Pathobiology, University of Illinois
at Urbana-Champaign, Urbana, Illinois 618022
Received 6 May 1999/Returned for modification 30 June 1999/Accepted 13 July 1999
In the murine model of Lyme disease, C3H/He mice exhibit severe
arthritis while C57BL/6N mice exhibit mild lesions when infected with
Borrelia burgdorferi. Joint tissues from these two strains of mice harbor similar concentrations of B. burgdorferi,
suggesting that the difference in disease severity reflects differences
in the magnitude of the inflammatory response to B. burgdorferi lipoproteins. Stimulation of bone marrow macrophages
from C3H/HeN mice with the B. burgdorferi lipoprotein OspA
resulted in higher-level production of the inflammatory mediators tumor
necrosis factor alpha, nitric oxide, and interleukin-6 (IL-6) than that
of macrophages from C57BL/6N mice. In contrast, macrophages from
C57BL/6N mice consistently produced larger amounts of the
anti-inflammatory cytokine IL-10 than did C3H/HeN macrophages. Addition
of recombinant IL-10 suppressed the production of inflammatory
mediators by macrophages from both strains. IL-10 was found to modulate
B. burgdorferi-induced inflammation in vivo, since C57BL/6J
mice deficient in IL-10 (IL-10
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Dual Role of Interleukin-10 in Murine Lyme Disease:
Regulation of Arthritis Severity and Host Defense
/
) developed more severe
arthritis than wild-type C57BL/6J mice. The increase in arthritis
severity was associated with a 10-fold decrease in the number of
B. burgdorferi organisms present in ankle tissues from
IL-10
/
mice. These findings suggest that in C57BL/6
mice, IL-10-dependent regulation of arthritis severity occurs at the
expense of effective control of bacterial numbers.
*
Corresponding author. Mailing address: Division of Cell
Biology and Immunology, Department of Pathology, University of Utah School of Medicine, 50 N. Medical Dr., Salt Lake City, UT 84132. Phone:
(801) 581-4364. Fax: (801) 581-4517. E-mail:
Mark.Wooten{at}path.med.utah.edu.
This article has been cited by other articles:
| J. Bacteriol. | J. Virol. | Eukaryot. Cell |
|---|
| Microbiol. Mol. Biol. Rev. | Clin. Vaccine Immunol. | All ASM Journals |
|---|