BACKGROUND: Severe periodontal breakdown is often associated with Down syndrome (DS); however, the etiology of this condition is not understood fully. Cellular motility of gingival fibroblasts is a critical event for wound healing and regeneration of periodontal tissues. Porphyromonas gingivalis is known to be a periodontal pathogen that invades host cells, contributing to periodontal destruction. In this study, we examined the influence of P. gingivalis infection on the motility of DS gingival fibroblasts (DGFs). METHODS: DGFs and normal gingival fibroblasts (NGFs) were infected with P. gingivalis with type II fimbriae, and cellular motility was evaluated using an in vitro wounding assay. Protein degradation of alpha5beta1-integrin subunits and a migration-regulating signaling molecule, paxillin, were investigated using specific antibodies. The adhesion to and invasion of fibroblasts by P. gingivalis were determined with a colony forming assay. The gene expressions of alpha5beta1-integrin subunits were also quantified using a reverse transcription-polymerase chain reaction method. RESULTS: The cellular motility of DGFs was impaired significantly by P. gingivalis compared to NGFs, and the former were invaded readily by P. gingivalis. Further, cellular paxillin from DGFs was degraded markedly by the pathogen. Although protein degradation of alpha5beta1 integrin was induced, its mRNA expression was not affected significantly. CONCLUSIONS: P. gingivalis readily invades DGFs and subsequently degrades paxillin, which impairs cellular motility and likely prevents wound healing and the regeneration of periodontal tissues. These characteristics may be involved in the etiology of DS periodontitis.
BACKGROUND: Severe periodontal breakdown is often associated with Down syndrome (DS); however, the etiology of this condition is not understood fully. Cellular motility of gingival fibroblasts is a critical event for wound healing and regeneration of periodontal tissues. Porphyromonas gingivalis is known to be a periodontal pathogen that invades host cells, contributing to periodontal destruction. In this study, we examined the influence of P. gingivalis infection on the motility of DS gingival fibroblasts (DGFs). METHODS: DGFs and normal gingival fibroblasts (NGFs) were infected with P. gingivalis with type II fimbriae, and cellular motility was evaluated using an in vitro wounding assay. Protein degradation of alpha5beta1-integrin subunits and a migration-regulating signaling molecule, paxillin, were investigated using specific antibodies. The adhesion to and invasion of fibroblasts by P. gingivalis were determined with a colony forming assay. The gene expressions of alpha5beta1-integrin subunits were also quantified using a reverse transcription-polymerase chain reaction method. RESULTS: The cellular motility of DGFs was impaired significantly by P. gingivalis compared to NGFs, and the former were invaded readily by P. gingivalis. Further, cellular paxillin from DGFs was degraded markedly by the pathogen. Although protein degradation of alpha5beta1 integrin was induced, its mRNA expression was not affected significantly. CONCLUSIONS:P. gingivalis readily invades DGFs and subsequently degrades paxillin, which impairs cellular motility and likely prevents wound healing and the regeneration of periodontal tissues. These characteristics may be involved in the etiology of DS periodontitis.
Authors: M H Tanaka; T O Rodrigues; L S Finoti; S R L Teixeira; M P A Mayer; R M Scarel-Caminaga; E M A Giro Journal: Eur J Clin Microbiol Infect Dis Date: 2014-11-04 Impact factor: 3.267