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Infection and Immunity, November 2008, p. 5120-5126, Vol. 76, No. 11
0019-9567/08/$08.00+0     doi:10.1128/IAI.00228-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Staphylococcus aureus Induces Expression of Receptor Activator of NF-{kappa}B Ligand and Prostaglandin E2 in Infected Murine Osteoblasts{triangledown}

Shankari N. Somayaji, Samantha Ritchie, Mahnaz Sahraei, Ian Marriott, and Michael C. Hudson*

Department of Biology, University of North Carolina at Charlotte, Charlotte, North Carolina

Received 18 February 2008/ Returned for modification 19 April 2008/ Accepted 22 August 2008

Osteomyelitis is an inflammatory disease of the bone that is characterized by the presence of necrotic bone tissue and increased osteoclast activity. Staphylococcus aureus is responsible for approximately 80% of all cases of human osteomyelitis. While the disease is especially difficult to treat, the pathogenesis of S. aureus-induced osteomyelitis is poorly understood. Elucidating the molecular mechanisms by which S. aureus induces osteomyelitis could lead to a better understanding of the disease and its progression and development of new treatments. Osteoblasts can produce several soluble factors that serve to modulate the activity or formation of osteoclasts. Receptor activator of NF-{kappa}B ligand (RANK-L) and prostaglandin E2 (PGE2) are two such molecules which can promote osteoclastogenesis and stimulate bone resorption. In addition, previous studies in our laboratory have shown that osteoblasts produce inflammatory cytokines, such as interleukin 6, following infection with S. aureus, which could induce COX-2 and in turn PGE2, further modulating osteoclast recruitment and differentiation. Therefore, we hypothesized that following infection with S. aureus, osteoblasts will express increased levels of RANK-L and PGE2. The results presented in this study provide evidence for the first time that RANK-L mRNA and protein and PGE2 expression are upregulated in S. aureus-infected primary osteoblasts. In addition, through the use of the specific COX-2 inhibitor NS 398, we show that when PGE2 production is inhibited, RANK-L production is decreased. These data suggest a mechanism whereby osteoblasts regulate the production of RANK-L during infection.

* Corresponding author. Mailing address: Department of Biology, University of North Carolina at Charlotte, 9201 University City Boulevard, Charlotte, NC 28223. Phone: (704) 687-8694. Fax: (704) 687-3128. E-mail: mchudson{at}uncc.edu

{triangledown} Published ahead of print on 2 September 2008.

Editor: S. R. Blanke

Infection and Immunity, November 2008, p. 5120-5126, Vol. 76, No. 11
0019-9567/08/$08.00+0     doi:10.1128/IAI.00228-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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