Interleukin 15 Mediates Joint Destruction in Staphylococcus Aureus Arthritis
Artikel i vetenskaplig tidskrift, 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

Författare

Louise Henningsson

Göteborgs universitet

Pernilla Jirholt

Göteborgs universitet

Yalda Rahpeymai Bogestål

Göteborgs universitet

Tove Eneljung

Göteborgs universitet

Martin Adiels

Göteborgs universitet

Catharina Lindholm

Göteborgs universitet

I. McInnes

S. Bulfone-Paus

Ulf H Lerner

Göteborgs universitet

Inger Gjertsson

Göteborgs universitet

Journal of Infectious Diseases

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

Vol. 206 687-696

Ämneskategorier

Reumatologi och inflammation

DOI

10.1093/infdis/jis295