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Infection and Immunity, October 2003, p. 6019-6026, Vol. 71, No. 10
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.10.6019-6026.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Streptococcus pyogenes Infection Induces Septic Arthritis with Increased Production of the Receptor Activator of the NF-{kappa}B Ligand

Atsuo Sakurai,1,2 Nobuo Okahashi,1,3* Ichiro Nakagawa,1 Shigetada Kawabata,1,4 Atsuo Amano,3 Takashi Ooshima,2 and Shigeyuki Hamada1

Departments of Oral and Molecular Microbiology,1 Pediatric Dentistry,2 Oral Frontier Biology, Osaka University Graduate School of Dentistry, Suita-Osaka 565-0871,3 PRESTO, Japan Science and Technology Corporation, Kawaguchi-Saitama 332-0012, Japan4

Received 18 April 2003/ Returned for modification 17 June 2003/ Accepted 18 July 2003

Bacterial arthritis is a rapidly progressive and highly destructive joint disease in humans, with Staphylococcus aureus and Neisseria gonorrhoeae the major causative agents, although beta-hemolytic streptococci as well often induce the disease. We demonstrate here that intravenous inoculation of CD-1 mice with the group A streptococcus (GAS) species Streptococcus pyogenes resulted in a high incidence of septic arthritis. Signs of arthritis emerged within the first few days after injection, and bacterial examinations revealed that colonization of the inoculated GAS in the arthritic joints persisted for 21 days. Induction of persistent septic arthritis was dependent on the number of microorganisms inoculated. Immunohistochemical staining of GAS with anti-GAS antibodies revealed colonization in the joints of infected mice. Cytokine levels were quantified in the joints and sera of infected mice by using an enzyme-linked immunosorbent assay. High levels of interleukin-1ß (IL-1ß) and IL-6 were detected in the joints from 3 to 20 days after infection. We noted that an increase in the amount of receptor activator of NF-{kappa}B ligand (RANKL), which is a key cytokine in osteoclastogenesis, was also evident in the joints of the infected mice. RANKL was not detected in sera, indicating local production of RANKL in the infected joints. Blocking of RANKL by osteoprotegerin, a decoy receptor of RANKL, prevented bone destruction in the infected joints. These results suggest that GAS can colonize in the joints and induce bacterial arthritis. Local RANKL production in the infected joints may be involved in bone destruction.

* Corresponding author. Mailing address: Department of Oral Frontier Biology, Osaka University Graduate School of Dentistry, 1-8, Yamadaoka, Suita-Osaka 565-0871, Japan. Phone: 81-6-6879-2976. Fax: 81-6-6879-2976. E-mail: okahashi{at}dent.osaka-u.ac.jp.

Editor: J. N. Weiser

Infection and Immunity, October 2003, p. 6019-6026, Vol. 71, No. 10
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.10.6019-6026.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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