第94回日本細菌学会総会

講演情報

オンデマンド口頭発表(ODP)

6 病原因子と生体防御

[ODP6B] b. 毒素・エフェクター・生理活性物質

[ODP-152] Porphyromonas gingivalisジンジパインによるヒト血管内皮細胞のPAI-1分解作用

○Liting Song1,松下 健二2,多田 浩之1 (1東北大・歯・口腔分子制御,2国立長寿医療セ・口腔疾患)

Objectives: The key pathogen associated with chronic periodontitis is Porphyromonas gingivalis, whose gingipains, cysteine proteinases, are key virulence factors of the disease. Plasminogen activator inhibitor-1 (PAI-1) is an important component of the coagulation system that downregulates fibrinolysis in the circulation. Reduced PAI-1 levels result in increased fibrinolysis and associated bleeding diathesis. We investigated the role of P. gingivalis infection on the production of PAI-1 by human endothelial cells.
Methods: Human umbilical vein endothelial cells (HUVECs) were cultured in EBM-2 supplemented with growth factors and then used after six passages. HUVECs were stimulated with viable or lyophilized whole cells of the P. gingivalis ATCC 33277, W83 wild-type, or gingipain-null mutant KDP136.
Results: Incubation of HUVECs with viable or lyophilized whole cells of P. gingivalis ATCC 33277 or W83 led to decrease PAI-1 production. However, PAI-1 mRNA levels did not decrease in the cells infected with P. gingivalis. Furthermore, a decrease in PAI-1 production was not observed in HUVECs infected with P. gingivalis KDP136.
Conclusion: These findings suggest that P. gingivalis infection probably causes cleavage of PAI-1 produced by endothelial cells and may contribute to the associated bleeding diathesis in periodontal tissues.