title: Interleukin 15 mediates joint destruction in Staphylococcus aureus arthritis.
abstract: 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.
authors.affiliation: Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy University of Gothenburg, Gothenburg, Sweden.
authors.forename: Louise
authors.initials: L
authors.lastname: Henningsson
authors.forename: Pernilla
authors.initials: P
authors.lastname: Jirholt
authors.forename: Yalda Rahpeymai
authors.initials: YR
authors.lastname: Bogestål
authors.forename: Tove
authors.initials: T
authors.lastname: Eneljung
authors.forename: Martin
authors.initials: M
authors.lastname: Adiels
authors.forename: Catharina
authors.initials: C
authors.lastname: Lindholm
authors.forename: Iain
authors.initials: I
authors.lastname: McInnes
authors.forename: Silvia
authors.initials: S
authors.lastname: Bulfone-Paus
authors.forename: Ulf H
authors.initials: UH
authors.lastname: Lerner
authors.forename: Inger
authors.initials: I
authors.lastname: Gjertsson
mesh_terms: D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood; D001170:Arthritis, Infectious / Q000276:immunology* / Q000382:microbiology*; D005260:Female; D055786:Gene Knockout Techniques; D006651:Histocytochemistry; D019409:Interleukin-15 / Q000097:blood / Q000172:deficiency / Q000235:genetics / Q000276:immunology*; D007596:Joints / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D053208:Kaplan-Meier Estimate; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010010:Osteoclasts / Q000201:enzymology / Q000276:immunology / Q000473:pathology; D013203:Staphylococcal Infections / Q000276:immunology* / Q000382:microbiology; D013211:Staphylococcus aureus / Q000302:isolation & purification*
chemical_list: D000907:Antibodies, Bacterial; D019409:Interleukin-15