IMR Press / FBL / Volume 13 / Issue 1 / DOI: 10.2741/2668

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


Porphyromonas gingivalis and the autophagic pathway: an innate immune interaction?

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1 Department of Oral Biology, College of Dentistry, Center for Molecular Microbiology, University of Florida, Gainesville, Florida 32610
2 Department of Anatomy and Cell Biology, College of Medicine, and Center for Molecular Microbiology, University of Florida, Gainesville, Florida 32610
Front. Biosci. (Landmark Ed) 2008, 13(1), 178–187;
Published: 1 January 2008

Autophagy is a mechanism used to maintain several intracellular functions essential to eukaryotic cells. Recently, a role for autophagy in innate and adaptive immunity has also been established including the elimination of invading bacteria. Although some intracellular pathogens are killed by autophagy, several others subvert autophagy to the pathogen's benefit for survival and replication. Porphyromonas gingivalis, an important periodontal pathogen, has been shown to stimulate autophagy in endothelial cells and to use the autophagic pathway to its advantage. In human coronary artery endothelial cells (HCAEC), P. gingivalis localizes within autophagosomes. After intracellular uptake, P. gingivalis transits from early autophagosomes to late autophagosomes and prevents the formation of autolysosomes, either by delaying the autophagosome-lysosome fusion or by redirecting the normal autophagic trafficking. In addition, P. gingivalis was also found to stimulate autophagy in human aortic endothelial cells (HAEC) since co-localization of LC3-II, an autophagosome marker, with P. gingivalis was observed. The trafficking of P. gingivalis into the autophagic pathway appears to be dependent upon the host cell type. Survival of P. gingivalis through the subversion of the host autophagic pathway can be considered a bacterial strategy to evade the innate immune system and persist in the host.

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