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Infection and Immunity, September 2001, p. 5698-5708, Vol. 69, No. 9
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.9.5698-5708.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Porphyromonas gingivalis Traffics to Autophagosomes in Human Coronary Artery Endothelial Cells

Brian R. Dorn,1,2 William A. Dunn Jr.,1,3 and Ann Progulske-Fox1,2,*

Center for Molecular Microbiology,1 Department of Oral Biology, College of Dentistry,2 and Department of Anatomy and Cell Biology,3 College of Medicine, University of Florida, Gainesville, Florida 32610

Received 18 January 2001/Returned for modification 21 March 2001/Accepted 4 June 2001

Porphyromonas gingivalis is a periodontal pathogen that also localizes to atherosclerotic plaques. Our previous studies demonstrated that P. gingivalis is capable of invading endothelial cells and that intracellular bacteria are contained in vacuoles that resemble autophagosomes. In this study, we have examined the trafficking of P. gingivalis 381 to the autophagic pathway. P. gingivalis 381 internalized by human coronary artery endothelial (HCAE) cells is located within vacuoles morphologically identical to autophagosomes. The progression of P. gingivalis 381 through intracellular vacuoles was analyzed by immunofluorescence microscopy. Vacuoles containing P. gingivalis colocalize with Rab5 and HsGsa7p early after internalization. At later times, P. gingivalis colocalizes with BiP and then progresses to a vacuole that contains BiP and lysosomal glycoprotein 120. Late endosomal markers and the lysosomal cathepsin L do not colocalize with P. gingivalis 381. The intracellular survival of P. gingivalis 381 decreases over 8 h in HCAE cells pretreated with the autophagy inhibitors 3-methyladenine and wortmannin. In addition, the vacuole containing P. gingivalis 381 lacks BiP but contains cathepsin L in the presence of wortmannin. These results suggest that P. gingivalis 381 evades the endocytic pathway to lysosomes and instead traffics to the autophagosome.

* Corresponding author. Department of Oral Biology, University of Florida, P.O. Box 100424, Gainesville, FL 32610-0424. Phone: (352) 846-0770. Fax: (352) 392-2361. E-mail: apfox{at}dental.ufl.edu.

Infection and Immunity, September 2001, p. 5698-5708, Vol. 69, No. 9
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.9.5698-5708.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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