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Interleukin 15 Mediates Joint Destruction in Staphylococcus Aureus Arthritis

Journal article
Authors Louise Henningsson
Pernilla Jirholt
Yalda Rahpeymai Bogestål
Tove Eneljung
Martin Adiels
Catharina Lindholm
I. McInnes
S. Bulfone-Paus
Ulf H Lerner
Inger Gjertsson
Published in Journal of Infectious Diseases
Volume 206
Issue 5
Pages 687-696
ISSN 0022-1899
Publication year 2012
Published at Wallenberg Laboratory
Institute of Medicine, Department of Rheumatology and Inflammation Research
Centre for Bone and Arthritis Research
Pages 687-696
Language en
Keywords natural-killer-cells, rheumatoid-arthritis, bone-resorption, deficient, mice, in-vivo, il-15, receptor, osteoclasts, model, stimulation
Subject categories Rheumatology and Autoimmunity


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.

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