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Journal of Clinical Microbiology, March 2004, p. 1149-1154, Vol. 42, No. 3
0095-1137/04/$08.00+0     DOI: 10.1128/JCM.42.3.1149-1154.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Translocation of Enterococcus faecalis Strains across a Monolayer of Polarized Human Enterocyte-Like T84 Cells

Jing Zeng,1,2 Fang Teng,1,2 George M. Weinstock,2,3,{dagger} and Barbara E. Murray1,2,3*

Division of Infectious Diseases, Department of Medicine,1 Center for the Study of Emerging and Re-emerging Pathogens,2 Department of Microbiology and Molecular Genetics, University of Texas, Houston, Texas 770303

Received 12 September 2003/ Returned for modification 15 October 2003/ Accepted 18 November 2003

We used a two-chamber system to study transcytosis of Enterococcus faecalis across monolayers of human colon carcinoma-derived T84 cells, which show structural resemblance to the native intestine. Among 16 E. faecalis isolates from different sources, the well-characterized strain OG1RF and 8 other isolates (2 endocarditis isolates, 1 urine isolate, and all 5 fecal isolates) showed translocation in this assay, while 6 clinical isolates (3 endocarditis and 3 urine isolates), the recipient strain JH2-2, and the control, Escherichia coli DH5{alpha}, had no detectable translocation. Of two OG1RF mutants involving the previously studied epa (enterococcal polysaccharide antigen) gene cluster, known to be needed for virulence and resistance to killing by polymorphonuclear leukocytes, one epa mutant (TX5179) was unable to translocate, while TX5180, with an epa disruption farther downstream, showed a moderate decrease in translocation relative to that of the wild-type strain OG1RF (P < 0.01), indicating that the epa gene cluster is important for translocation across a T84 monolayer. This observation was confirmed by complementation of the epa mutant (TX5179) with epa genes and restoration of its translocation ability. In conclusion, we have demonstrated translocation of at least some strains of E. faecalis across T84 monolayers, although strains differ considerably in this ability, and we have demonstrated that epa mutations can cause marked changes in successful translocation. These results suggest that this model may be a useful in vitro system for studying the process of translocation from the intestinal tract.

* Corresponding author. Mailing address: Center for the Study of Emerging and Re-emerging Pathogens, Division of Infectious Diseases, 1728 JFB, University of Texas Medical School, 6431 Fannin St., Houston, TX 77030. Phone: (713) 500-6745. Fax: (713) 500-6766. E-mail: BEM.asst{at}uth.tmc.edu.

{dagger} Present address: Human Genome Sequencing Center, Baylor College of Medicine, Houston, TX 77030.

Journal of Clinical Microbiology, March 2004, p. 1149-1154, Vol. 42, No. 3
0095-1137/04/$08.00+0     DOI: 10.1128/JCM.42.3.1149-1154.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Teng, F., Singh, K. V., Bourgogne, A., Zeng, J., Murray, B. E. (2009). Further Characterization of the epa Gene Cluster and Epa Polysaccharides of Enterococcus faecalis. Infect. Immun. 77: 3759-3767 [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]  


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