Interleukin-10 (IL-10) inhibits Borrelia burgdorferi-induced IL-17 production and attenuates IL-17-mediated Lyme arthritis.
Infect Immun
; 81(12): 4421-30, 2013 Dec.
Article
in En
| MEDLINE
| ID: mdl-24042116
ABSTRACT
Previous studies have shown that cells and cytokines associated with interleukin-17 (IL-17)-driven inflammation are involved in the arthritic response to Borrelia burgdorferi infection. Here, we report that IL-17 is a contributing factor in the development of Lyme arthritis and show that its production and histopathological effects are regulated by interleukin-10 (IL-10). Spleen cells obtained from B. burgdorferi-infected, "arthritis-resistant" wild-type C57BL/6 mice produced low levels of IL-17 following stimulation with the spirochete. In contrast, spleen cells obtained from infected, IL-10-deficient C57BL/6 mice produced a significant amount of IL-17 following stimulation with B. burgdorferi. These mice developed significant arthritis, including erosion of the bones in the ankle joints. We further show that treatment with antibody to IL-17 partially inhibited the significant hind paw swelling and histopathological changes observed in B. burgdorferi-infected, IL-10-deficient mice. Taken together, these findings provide additional evidence of a role for IL-17 in Lyme arthritis and reveal an additional regulatory target of IL-10 following borrelial infection.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Arthritis
/
Lyme Disease
/
Interleukin-10
/
Interleukin-17
/
Borrelia burgdorferi
Limits:
Animals
Language:
En
Journal:
Infect Immun
Year:
2013
Document type:
Article
Affiliation country:
United States