Interleukin 15 Mediates Joint Destruction in Staphylococcus Aureus Arthritis
Journal article, 2012

Background. Staphylococcus aureus arthritis causes severe and rapid joint damage despite antibiotics. Thus, there is a need to identify new treatment targets in addition to antibiotics. Lately, interleukin 15 (IL-15) has been implicated both in osteoclastogenesis and in bacterial clearance-2 important issues in S. aureus-induced joint destruction. This has prompted us to investigate the importance of IL-15 in S. aureus-induced arthritis. Methods.Toxic shock syndrome toxin-1 producing S. aureus was intravenously inoculated in IL-15 knockout and wildtype mice and in wildtype mice treated with anti-IL-15 antibodies (aIL-15ab) or isotype control antibody. Results.Absence of IL-15, either in knockout mice or after treatment with aIL-15ab, significantly reduced weight loss compared with controls during the infection. The severity of synovitis and joint destruction was significantly decreased in IL-15 knockout and aIL-15ab treated mice compared with controls. In IL-15 knockout mice there was a reduced number of osteoclasts in the joints. The host's ability to clear bacteria was not influenced in the IL-15 knockout mice, but significantly increased after treatment with aIL-15ab. Conclusions.IL-15 is a mediator of joint destruction in S. aureus-induced arthritis and contributes to general morbidity, which makes this cytokine an interesting treatment target in addition to conventional antibiotics.

mice

osteoclasts

bone-resorption

in-vivo

model

il-15

rheumatoid-arthritis

stimulation

natural-killer-cells

deficient

receptor

Author

Louise Henningsson

University of Gothenburg

Pernilla Jirholt

University of Gothenburg

Yalda Rahpeymai Bogestål

University of Gothenburg

Tove Eneljung

University of Gothenburg

Martin Adiels

University of Gothenburg

Catharina Lindholm

University of Gothenburg

I. McInnes

S. Bulfone-Paus

Ulf H Lerner

University of Gothenburg

Inger Gjertsson

University of Gothenburg

Journal of Infectious Diseases

0022-1899 (ISSN) 1537-6613 (eISSN)

Vol. 206 5 687-696

Subject Categories

Rheumatology and Autoimmunity

DOI

10.1093/infdis/jis295

More information

Created

10/10/2017