A role for fimbriae in Porphyromonas gingivalis invasion of oral epithelial cells

Abstract

Isogenic mutants of Porphyromonas gingivalis which differ in the expression of fimbriae were used to examine the contribution of fimbriae in invasion of a human oral epithelial cell line (KB). At a multiplicity of infection of 100, the wild-type P. gingivalis strains 33277, 381, and A7436 exhibited adherence efficiencies of 5.5, 0.11, and 5.0%, respectively, and invasion efficiencies of 0.15, 0.03, and 0.10%, respectively. However, adherence to and invasion of KB cells was not detected with the P. gingivalis fimA mutants, DPG3 and MPG1. Adherence of P. gingivalis wild-type strains to KB cells was completely inhibited by the addition of hyperimmune sera raised to the major fimbriae. Examination by electron microscopy of invasion of epithelial cells by the P. gingivalis wild-type strain 381 revealed microvillus-like extensions around adherent bacteria; this was not observed with P. gingivalis fim mutants. Taken together, these results indicate that the P. gingivalis major fimbriae are required for adherence to and invasion of oral epithelial cells.

Fimbria-dependent activation of pro-inflammatory molecules in Porphyromonas gingivalis infected human aortic endothelial cells

“…As mentioned previously, the interaction of P. gingivalis with host cells has been described as a two-stage process of initial attachment mediated by the 41 kDa major fimbria, followed by more intimate attachment facilitating endocytosis of the bacteria (Lamont and Jenkinson, 1988;Njoroge et al, 1997). In addition, it has been demonstrated that expression of Fim A is not sufficient for invasion and that other surface molecules may be involved (Dorn et al, 2000).…”

“…Porphyromonas gingivalis attachment to host cells has been suggested to be a bi-phasic process whereby the major fimbria is responsible for initially tethering the bacteria to the host cell (Lamont and Jenkinson, 1988;Njoroge et al ., 1997). The exact mechanism by which more intimate attachment occurs is currently undefined.…”

Adhesion of Porphyromonas gingivalis. Serotypes to Pocket Epithelium

“…More than 98% of the adhering bac- briae-which affects the surface hydrophobicity-and not to the capsular type. 2,5,8,14 Bacterial capsules are composed of extracellular, hydrophilic, and negatively charged acidic polysaccharides. Encapsulation of P. gingivalis strains results in increased resistance to phagocytosis 15 and prevents activation of complement by shielding the P. gingivalis lipopolysaccharide.…”

Polymersome‐mediated intracellular delivery of antibiotics to treat Porphyromonas gingivalis ‐infected oral epithelial cells

“…gingivalis can adhere to and rapidly invade oral epithelial cells (4 -6). The initial attachment and subsequent invasion of P. gingivalis into epithelial cells is thought to be mediated by the major fimbriae of the bacterium, which bind to the integrin ␣5␤1 expressed within lipid rafts on the cell surface of host cells (7)(8)(9)(10). However, evidence indicates that other molecules are involved in or modulate the adhesion process.…”