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Infection and Immunity, September 2001, p. 5235-5242, Vol. 69, No. 9
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.9.5235-5242.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Involvement of Mitogen-Activated Protein Kinase Pathways in Staphylococcus aureus Invasion of Normal Osteoblasts

John K. Ellington, Adam Elhofy, Kenneth L. Bost, and Michael C. Hudson*

Department of Biology, University of North Carolina at Charlotte, Charlotte, North Carolina 28223

Received 16 January 2001/Returned for modification 2 March 2001/Accepted 25 May 2001

Staphylococcus aureus invades osteoblasts and can persist in the intracellular environment. The present study examined the role of osteoblast mitogen-activated protein kinase (MAPK) pathways in bacterial invasion. S. aureus infection of normal human and mouse osteoblasts resulted in an increase in the phosphorylation of the extracellular signal-regulated protein kinases (ERK 1 and 2). This stimulation of ERK 1 and 2 correlated with the time course of S. aureus invasion, and bacterial adherence induced the MAPK pathway. ERK 1 and 2 phosphorylation was time and dose dependent and required active S. aureus gene expression for maximal induction. The nonpathogenic Staphylococcus carnosus was also able to induce ERK 1 and 2 phosphorylation, albeit at lower levels than S. aureus. Phosphorylation of the stress-activated protein kinases was increased in both infected human and mouse osteoblasts; however, the p38 MAPK pathway was not activated in response to S. aureus. Finally, the transcription factor c-Jun, but not Elk-1 or ATF-2, was phosphorylated in response to S. aureus infection.

* Corresponding author. Mailing address: Department of Biology, University of North Carolina at Charlotte, 9201 University City Blvd., Charlotte, NC 28223. Phone: (704) 687-4048. Fax: (704) 687-3128. E-mail: mchudson{at}emailuncc.edu.

Infection and Immunity, September 2001, p. 5235-5242, Vol. 69, No. 9
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.9.5235-5242.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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