title: Arthritis is developed in Borrelia-primed and -infected mice deficient of interleukin-17.
abstract: 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-γ) levels in sera and increased frequencies of IFN-γ-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-γ.
authors: Wisconsin State Laboratory of Hygiene, University of Wisconsin-Madison, Madison, WI 53706, USA Department of Pathobiological Sciences, University of Wisconsin-Madison, Madison, WI 53706, USA kuo1@wisc.edu.
authors: Joseph
authors: J
authors: Kuo
authors: Department of Pathology and Laboratory Medicine, University of Wisconsin-Madison, Madison, WI 53706, USA.
authors: Thomas F
authors: TF
authors: Warner
authors: Department of Clinical Laboratory Science, Marquette University, Milwaukee, WI 53201, USA.
authors: Erik L
authors: EL
authors: Munson
authors: Department of Biomedical Sciences, University of Wisconsin-Milwaukee, Milwaukee, WI 53211, USA.
authors: Dean T
authors: DT
authors: Nardelli
authors: Wisconsin State Laboratory of Hygiene, University of Wisconsin-Madison, Madison, WI 53706, USA Department of Pathobiological Sciences, University of Wisconsin-Madison, Madison, WI 53706, USA Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, WI 53706, USA.
authors: Ronald F
authors: RF
authors: Schell
mesh_terms: D000818:Animals; D001168:Arthritis / Q000235:genetics* / Q000382:microbiology* / Q000473:pathology; D001898:Borrelia; D004195:Disease Models, Animal; D004487:Edema / Q000473:pathology; D015870:Gene Expression; D007371:Interferon-gamma / Q000097:blood / Q000378:metabolism; D020381:Interleukin-17 / Q000172:deficiency* / Q000235:genetics / Q000378:metabolism; D008193:Lyme Disease / Q000235:genetics* / Q000382:microbiology* / Q000473:pathology; D008198:Lymph Nodes / Q000276:immunology / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout
chemical_list: D020381:Interleukin-17; D007371:Interferon-gamma
keywords: Borrelia burgdorferi; Lyme arthritis; T cells; gamma-interferon; interleukin-17