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Intracellular survival and vascular cell-to-cell transmission of Porphyromonas gingivalis
BACKGROUND: Porphyromonas gingivalis is associated with periodontal disease and invades different cell types including epithelial, endothelial and smooth muscle cells. In addition to P. gingivalis DNA, we have previously identified live invasive bacteria in atheromatous tissue. However, the mechanis...
Autores principales: | , , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2008
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2259307/ https://www.ncbi.nlm.nih.gov/pubmed/18254977 http://dx.doi.org/10.1186/1471-2180-8-26 |
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author | Li, Ling Michel, Raynald Cohen, Joshua DeCarlo, Arthur Kozarov, Emil |
author_facet | Li, Ling Michel, Raynald Cohen, Joshua DeCarlo, Arthur Kozarov, Emil |
author_sort | Li, Ling |
collection | PubMed |
description | BACKGROUND: Porphyromonas gingivalis is associated with periodontal disease and invades different cell types including epithelial, endothelial and smooth muscle cells. In addition to P. gingivalis DNA, we have previously identified live invasive bacteria in atheromatous tissue. However, the mechanism of persistence of this organism in vascular tissues remains unclear. Therefore, the objective of this study was to analyze the ability of intracellular P. gingivalis to persist for extended periods of time, transmit to and possibly replicate in different cell types. RESULTS: Using antibiotic protection assays, immunofluorescent and laser confocal microscopy, we found that after a prolonged intracellular phase, while P. gingivalis can still be detected by immunostaining, the intracellular organisms lose their ability to be recovered in vitro. Surprisingly however, intracellular P. gingivalis could be recovered in vitro upon co incubation with fresh vascular host cells. We then demonstrated that the organism was able to exit the initially infected host cells, then enter and multiply in new host cells. Further, we found that cell-to-cell contact increased the transmission rate but was not required for transmission. Finally, we found that the invasion of new host cells allowed P. gingivalis to increase its numbers. CONCLUSION: Our results suggest that the persistence of vascular tissue-embedded P. gingivalis is due to its ability to transmit among different cell types. This is the first communication demonstrating the intercellular transmission as a likely mechanism converting latent intracellular bacteria from state of dormancy to a viable state allowing for persistence of an inflammatory pathogen in vascular tissue. |
format | Text |
id | pubmed-2259307 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2008 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-22593072008-03-04 Intracellular survival and vascular cell-to-cell transmission of Porphyromonas gingivalis Li, Ling Michel, Raynald Cohen, Joshua DeCarlo, Arthur Kozarov, Emil BMC Microbiol Research Article BACKGROUND: Porphyromonas gingivalis is associated with periodontal disease and invades different cell types including epithelial, endothelial and smooth muscle cells. In addition to P. gingivalis DNA, we have previously identified live invasive bacteria in atheromatous tissue. However, the mechanism of persistence of this organism in vascular tissues remains unclear. Therefore, the objective of this study was to analyze the ability of intracellular P. gingivalis to persist for extended periods of time, transmit to and possibly replicate in different cell types. RESULTS: Using antibiotic protection assays, immunofluorescent and laser confocal microscopy, we found that after a prolonged intracellular phase, while P. gingivalis can still be detected by immunostaining, the intracellular organisms lose their ability to be recovered in vitro. Surprisingly however, intracellular P. gingivalis could be recovered in vitro upon co incubation with fresh vascular host cells. We then demonstrated that the organism was able to exit the initially infected host cells, then enter and multiply in new host cells. Further, we found that cell-to-cell contact increased the transmission rate but was not required for transmission. Finally, we found that the invasion of new host cells allowed P. gingivalis to increase its numbers. CONCLUSION: Our results suggest that the persistence of vascular tissue-embedded P. gingivalis is due to its ability to transmit among different cell types. This is the first communication demonstrating the intercellular transmission as a likely mechanism converting latent intracellular bacteria from state of dormancy to a viable state allowing for persistence of an inflammatory pathogen in vascular tissue. BioMed Central 2008-02-06 /pmc/articles/PMC2259307/ /pubmed/18254977 http://dx.doi.org/10.1186/1471-2180-8-26 Text en Copyright © 2008 Li et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Li, Ling Michel, Raynald Cohen, Joshua DeCarlo, Arthur Kozarov, Emil Intracellular survival and vascular cell-to-cell transmission of Porphyromonas gingivalis |
title | Intracellular survival and vascular cell-to-cell transmission of Porphyromonas gingivalis |
title_full | Intracellular survival and vascular cell-to-cell transmission of Porphyromonas gingivalis |
title_fullStr | Intracellular survival and vascular cell-to-cell transmission of Porphyromonas gingivalis |
title_full_unstemmed | Intracellular survival and vascular cell-to-cell transmission of Porphyromonas gingivalis |
title_short | Intracellular survival and vascular cell-to-cell transmission of Porphyromonas gingivalis |
title_sort | intracellular survival and vascular cell-to-cell transmission of porphyromonas gingivalis |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2259307/ https://www.ncbi.nlm.nih.gov/pubmed/18254977 http://dx.doi.org/10.1186/1471-2180-8-26 |
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