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Infection and Immunity, January 2008, p. 141-152, Vol. 76, No. 1
0019-9567/08/$08.00+0     doi:10.1128/IAI.00556-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Staphylococcus epidermidis saeR Is an Effector of Anaerobic Growth and a Mediator of Acute Inflammation{triangledown}

L. D. Handke,1,{dagger} K. L. Rogers,1 M. E. Olson,1 G. A. Somerville,3 T. J. Jerrells,1 M. E. Rupp,1,2 P. M. Dunman,1 and P. D. Fey1,2*

Departments of Pathology and Microbiology,1 Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska 68198,2 Department of Veterinary and Biomedical Sciences, University of Nebraska-Lincoln, Lincoln, Nebraska 685833

Received 17 April 2007/ Returned for modification 22 May 2007/ Accepted 14 October 2007

The saeRS two-component regulatory system regulates transcription of multiple virulence factors in Staphylococcus aureus. In the present study, we demonstrated that the saePQRS region in Staphylococcus epidermidis is transcriptionally regulated in a temporal manner and is arranged in a manner similar to that previously described for S. aureus. Studies using a mouse foreign body infection model demonstrated that the virulence of strain 1457 and the virulence of a mutant, strain 1457 saeR, were statistically equivalent. However, histological analyses suggested that the polymorphonuclear neutrophil response at 2 days postinfection was significantly greater in 1457-infected mice than in 1457 saeR-infected mice, demonstrating that SaeR influences the early, acute phases of infection. Microarray analysis demonstrated that a saeR mutation affected the transcription of 65 genes (37 genes were upregulated and 28 genes were downregulated); in particular, 8 genes that facilitate growth under anaerobic conditions were downregulated in 1457 saeR. Analysis of growth under anaerobic conditions demonstrated that 1457 saeR had a decreased growth rate compared to 1457. Further metabolic experiments demonstrated that 1457 saeR had a reduced capacity to utilize nitrate as a terminal electron acceptor and exhibited increased production of lactic acid in comparison to 1457. These data suggest that in S. epidermidis SaeR functions to regulate the transition between aerobic growth and anaerobic growth. In addition, when grown anaerobically, 1457 saeR appeared to compensate for the redox imbalance created by the lack of electron transport-mediated oxidation of NADH to NAD+ by increasing lactate dehydrogenase activity and the subsequent oxidation of NADH.

* Corresponding author. Mailing address: University of Nebraska Medical Center, 986280 Nebraska Medical Center, Omaha, NE 68198-6280. Phone and fax: (402) 559-4077. E-mail: pfey{at}unmc.edu

{triangledown} Published ahead of print on 22 October 2007.

Editor: J. B. Bliska

{dagger} Present address: Department of Molecular, Biology and Microbiology, Tufts University School of Medicine, 136 Harrison Ave., Boston, MA 02111.

Infection and Immunity, January 2008, p. 141-152, Vol. 76, No. 1
0019-9567/08/$08.00+0     doi:10.1128/IAI.00556-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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