Abstract

Gingival epithelial cells function as an innate host defense system to prevent intrusion by periodontal bacteria. Nevertheless, Porphyromonas gingivalis, the most well-known periodontal pathogen, can enter gingival epithelial cells and pass through the epithelial barrier into deeper tissues. P. gingivalis fimbriae specifically interact with α5β1-integrin of epithelial cells. The bacterium is then subsequently captured by cellular pseudopodia, which enables invagination through the endosomal pathway. This entry event requires host cellular dynamin, actin fibers, microtubules, and lipid rafts. Following passage through the epithelial barrier, intracellular P. gingivalis impairs integrin-related signaling molecules, paxillin, and focal adhesion kinase, which disables cellular migration and proliferation. Thereafter some intracellular bacteria are sorted to lytic compartments, including autolysosomes and late endosomes/lysosomes, while a considerable number of the remaining organisms are sorted to recycling endosomes, leading to bacterial exit from infected cells to neighboring cells, a mechanism of cell-to-cell spreading in periodontal tissue. This article addresses the remarkable strategies used by P. gingivalis to invade and exit from periodontal cells.

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