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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Engelbert, M.
Right arrow Articles by Gilmore, M. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Engelbert, M.
Right arrow Articles by Gilmore, M. S.

 Previous Article  |  Next Article 

Infection and Immunity, June 2004, p. 3628-3633, Vol. 72, No. 6
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.6.3628-3633.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Contribution of Gelatinase, Serine Protease, and fsr to the Pathogenesis of Enterococcus faecalis Endophthalmitis

Michael Engelbert,1,{dagger} Eleftherios Mylonakis,2,{dagger} Frederick M. Ausubel,3,4 Stephen B. Calderwood,2,5 and Michael S. Gilmore1,6*

Department of Microbiology and Immunology,1 Department of Ophthalmology, The University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma,6 Division of Infectious Diseases,2 Department of Molecular Biology, Massachusetts General Hospital,3 Department of Genetics,4 Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts5

Received 24 September 2003/ Returned for modification 4 December 2003/ Accepted 19 February 2004

Gelatinase and serine protease were found to contribute in concert to pathogenesis in a rabbit model of endophthalmitis. However, a mutant defective in the fsr regulator was observed to be more attenuated than a mutant rendered defective in the expression of gelatinase and serine protease as the result of a polar transposon insertion into the former. This increased attenuation suggests that there are possible additional pleiotropic effects of the defect in fsr on expression of traits contributing to the pathogenesis of enterococcal infection.

* Corresponding author. Mailing address: Department of Ophthalmology and Microbiology and Immunology, University of Oklahoma Health Sciences Center, 975 NE 10th St., Oklahoma City, OK 73104. Phone: (405) 271-1083. Fax: (405) 271-8651. E-mail: Michael-Gilmore{at}ouhsc.edu.

Editor: J. N. Weiser

{dagger} M.E. and E.M. contributed equally to this work

Infection and Immunity, June 2004, p. 3628-3633, Vol. 72, No. 6
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.6.3628-3633.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Coburn, P. S., Baghdayan, A. S., Dolan, G., Shankar, N. (2008). An AraC-Type Transcriptional Regulator Encoded on the Enterococcus faecalis Pathogenicity Island Contributes to Pathogenesis and Intracellular Macrophage Survival. Infect. Immun. 76: 5668-5676 [Abstract] [Full Text]  
  • Thomas, V. C., Thurlow, L. R., Boyle, D., Hancock, L. E. (2008). Regulation of Autolysis-Dependent Extracellular DNA Release by Enterococcus faecalis Extracellular Proteases Influences Biofilm Development. J. Bacteriol. 190: 5690-5698 [Abstract] [Full Text]  
  • Del Papa, M. F., Hancock, L. E., Thomas, V. C., Perego, M. (2007). Full Activation of Enterococcus faecalis Gelatinase by a C-Terminal Proteolytic Cleavage. J. Bacteriol. 189: 8835-8843 [Abstract] [Full Text]  
  • Mohamed, J. A., Huang, D. B. (2007). Biofilm formation by enterococci. J Med Microbiol 56: 1581-1588 [Abstract] [Full Text]  
  • Park, S. Y., Kim, K. M., Lee, J. H., Seo, S. J., Lee, I. H. (2007). Extracellular Gelatinase of Enterococcus faecalis Destroys a Defense System in Insect Hemolymph and Human Serum. Infect. Immun. 75: 1861-1869 [Abstract] [Full Text]  
  • Nakayama, J., Tanaka, E., Kariyama, R., Nagata, K., Nishiguchi, K., Mitsuhata, R., Uemura, Y., Tanokura, M., Kumon, H., Sonomoto, K. (2007). Siamycin Attenuates fsr Quorum Sensing Mediated by a Gelatinase Biosynthesis-Activating Pheromone in Enterococcus faecalis. J. Bacteriol. 189: 1358-1365 [Abstract] [Full Text]  
  • Mohamed, J. A., Murray, B. E. (2006). Influence of the fsr locus on biofilm formation by Enterococcus faecalis lacking gelE.. J Med Microbiol 55: 1747-1750 [Full Text]  
  • Bourgogne, A., Hilsenbeck, S. G., Dunny, G. M., Murray, B. E. (2006). Comparison of OG1RF and an Isogenic fsrB Deletion Mutant by Transcriptional Analysis: the Fsr System of Enterococcus faecalis Is More than the Activator of Gelatinase and Serine Protease.. J. Bacteriol. 188: 2875-2884 [Abstract] [Full Text]  
  • Singh, K. V., Nallapareddy, S. R., Nannini, E. C., Murray, B. E. (2005). Fsr-Independent Production of Protease(s) May Explain the Lack of Attenuation of an Enterococcus faecalis fsr Mutant Versus a gelE-sprE Mutant in Induction of Endocarditis. Infect. Immun. 73: 4888-4894 [Abstract] [Full Text]  
  • Zeng, J., Teng, F., Murray, B. E. (2005). Gelatinase Is Important for Translocation of Enterococcus faecalis across Polarized Human Enterocyte-Like T84 Cells. Infect. Immun. 73: 1606-1612 [Abstract] [Full Text]  
  • Carniol, K., Gilmore, M. S. (2004). Signal Transduction, Quorum-Sensing, and Extracellular Protease Activity in Enterococcus faecalis Biofilm Formation. J. Bacteriol. 186: 8161-8163 [Full Text]  


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