This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Coburn, P. S.
Right arrow Articles by Shankar, N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Coburn, P. S.
Right arrow Articles by Shankar, N.

 Previous Article  |  Next Article 

Infection and Immunity, December 2008, p. 5668-5676, Vol. 76, No. 12
0019-9567/08/$08.00+0     doi:10.1128/IAI.00930-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

An AraC-Type Transcriptional Regulator Encoded on the Enterococcus faecalis Pathogenicity Island Contributes to Pathogenesis and Intracellular Macrophage Survival{triangledown}

Phillip S. Coburn, Arto S. Baghdayan, GT Dolan, and Nathan Shankar*

Department of Pharmaceutical Sciences, The University of Oklahoma Health Sciences Center, P.O. Box 26901, Oklahoma City, Oklahoma 73126

Received 25 July 2008/ Returned for modification 2 September 2008/ Accepted 19 September 2008

A gene encoding a putative AraC-type transcriptional regulator was identified on the 153-kb pathogenicity island (PAI) found among virulent Enterococcus faecalis strains. In an effort to understand the function of this regulator, designated PerA (for pathogenicity island-encoded regulator), we first examined the expression of the perA gene in the original PAI strain MMH594 and in an unrelated clinical isolate E99 by reverse transcription-PCR. Interestingly, expression analysis revealed no detectable perA transcript in MMH594, whereas a transcript was observed in strain E99. Nucleotide sequence analysis revealed that this altered expression between the two strains was attributable to the differential location of an IS1191 element within the putative promoter region upstream of the perA gene. In order to determine the role of this putative regulator in E. faecalis pathogenesis, a perA-deficient mutant was created in strain E99, and the wild-type and mutant pair were compared for phenotypic differences. In in vitro biofilm assays, the mutant strain showed a significantly higher level of growth medium-specific biofilm formation compared to the wild type. However, in a murine intraperitoneal infection model, the mutant strain was significantly less pathogenic. The mutant was also attenuated for survival within macrophages in vitro. These findings highlight the importance of PerA as a regulator of biofilm formation and survival within macrophages and is likely a regulator controlling determinants important to pathogenesis.

* Corresponding author. Mailing address: Department of Pharmaceutical Sciences, The University of Oklahoma Health Sciences Center, P.O. Box 26901, Oklahoma City, OK 73126. Phone: (405) 271-6481. Fax: (405) 271-7505. E-mail: nathan-shankar{at}ouhsc.edu

{triangledown} Published ahead of print on 29 September 2008.

Editor: J. N. Weiser

Infection and Immunity, December 2008, p. 5668-5676, Vol. 76, No. 12
0019-9567/08/$08.00+0     doi:10.1128/IAI.00930-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»