Anti-Phagocytic Role of Surface Fibrous Structure of an Invasive Porphyromonas Gingivalis Strain

Abstract

Recent studies have shown that invasive and non-invasive strains of Porphyromonas gingivalis can both be isolated from patients with periodontitis. We examined the interaction between an invasive 16-1 P. gingivalis strain and phagocytes obtained from human peripheral blood and guinea pig peritoneal cavity. Phagocytes from human peripheral blood, mainly polymorphonuclear leukocytes (PMNs) isolated by centrifugation in Ficoll Hypaque, and macrophages collected from the peritoneal cavity of guinea pigs, were exposed to P. gingivalis cells. After this exposure, greater numbers of the non-invasive P. gingivalis ATCC 33277 were observed in human PMNs and guinea pig macrophages compared with the invasive P. gingivalis 16-1. Electron microscopic observations showed that invasive 16-1 within phagosomes in human PMNs and guinea pig macrophages retained their surface fibrous structures as well as their outer membranes. Electron microscopic examination showed that destruction and damage to the cell membranes and inner structures were clear in human PMNs and guinea pig macrophages after exposure to invasive 16-1 for 6 and 24 hours; this was a clear difference from exposure to the non-invasive ATCC 33277. Release of lactate dehydrogenase (LDH) activities into the culture supernatant of PMNs after exposure to the invasive 16-1 for 4 and 6 hours was significantly greater than that after exposure to the non-invasive ATCC 33277 (pϽ0.05). On the other hand, the LDH activity after exposure for 21 hours to the invasive 16-1 was significantly lower than that of untreated cells and cells after exposure to the non-invasive ATCC 33277 strain (pϽ0.05). The PMN viabilities after exposure to cells of the invasive 16-1 for 3, 4, and 6 hours as evaluated by trypan blue staining were similar to those after exposure to cells of the non-invasive ATCC 33277, but that after exposure to the invasive 16-1 strain for 21 hours was significantly lower than that after exposure to cells of the noninvasive ATCC 33277 strain.

Colocalization of Porphyromonas gingivalis with CD4+ T cells in periodontal disease

“…Because of its many virulence factors, such as proteases, P. gingivalis can modulate host cytokine signaling networks and generate inflammatory infiltrates that are responsible for the chronic nature of periodontitis. Previous studies have shown that P. gingivalis can survive, spread to neighboring host epithelial cells, and resist phagocytosis in vitro (Cutler et al ., ; Miyabe et al ., ). In vivo , P. gingivalis has been identified in pathological gingiva using several methods, including immunofluorescence, immunohistochemistry, and fluorescence in situ hybridization (Rudney et al ., ; Kim et al ., ).…”