Arthritis is developed in Borrelia-primed and -infected mice deficient of interleukin-17

作者：Kuo Joseph^*; Warner Thomas F; Munson Erik L; Nardelli Dean T; Schell Ronald F

来源：Pathogens and Disease, 2016, 74(7): ftw077.

DOI：10.1093/femspd/ftw077

• Lyme arthritis
• Borrelia burgdorferi
• interleukin-17
• gamma-interferon
• T cells

Interleukin-17 (IL-17) has been shown to participate in the development of Lyme arthritis in experimental mice. For example, neutralization of IL-17 with antibodies inhibits induction of arthritis in Borrelia-primed and -infected C57BL/6 wild-type mice. We hypothesized that mice lacking IL-17 would fail to develop Borrelia-induced arthritis. IL-17-deficient and wild-type C57BL/6 mice were primed with heat-inactivated Borrelia and then infected with viable spirochetes 3 weeks later. No swelling or major histopathological changes of the hind paws were detected in IL-17-deficient or wild-type mice that were primed with Borrelia or infected with viable spirochetes. By contrast, IL-17-deficient and wild-type mice that were primed and subsequently infected with heterologous Borrelia developed severe swelling and histopathological changes of the hind paws. In addition, Borrelia-primed and -infected IL-17-deficient mice exhibited elevated gamma-interferon (IFN-gamma) levels in sera and increased frequencies of IFN-gamma-expressing lymphocytes in popliteal lymph nodes compared to Borrelia-primed and -infected wild-type mice. These results demonstrate that IL-17 is not required for development of severe pathology in response to infection with Borrelia burgdorferi, but may contribute to disease through an interaction with IFN-gamma.Borrelia-induced arthritis in IL-17-deficient mice.Borrelia-induced arthritis in IL-17-deficient mice.

• 出版日期2016-10