[ODP6B] b. 毒素・エフェクター・生理活性物質

[ODP-144] P. gingivalisならびにF. nucleatum LPSはE. coli LPSによるヒト単球のIL-6産生を増強する

○坂本 雄哉^1,2，尾之上 さくら³，川原 一芳³，松下 健二⁴，多田 浩之² (¹東北大・歯，²東北大・歯・口腔分子制御，³関東学院大・理工・生命科学，⁴国立長寿医療セ・口腔疾患)

Objective: Periodontal disease is an inflammatory disease that often involves infection by the oral bacterial pathogen Porphyromonas gingivalis (Pg) or Fusobacterium nucleatum (Fn). Oral bacteria play ‍an essential role in the relationships between oral inflammation and susceptibility to systemic diseases. IL-6 is involved in the pathogenesis of numerous chronic infectious diseases. We investigated Escherichia coli (Ec) LPS-induced IL-6 production by macrophages primed with Pg LPS or Fn LPS. Methods: Human monocytic THP-1 cells were induced to differentiate into macrophages by maxacalcitol (OCT), a vitamin D₃ analog. Cells were pretreated with Pg or Fn LPS, washed, and then stimulated with Ec LPS. The IL-6 levels in the culture supernatants were measured by ELISA. Results: Priming with Pg or Fn LPS augmented Ec LPS-induced IL-6 production in THP-1 cell cultures. The alteration of IL-6 by Pg or Fn LPS priming was inhibited by ERK, JNK, or p38 inhibitors. However, TLR2 ligand priming was unable to augment Ec LPS-induced IL-6 production. Conclusion: This study suggests that Ec LPS-induced IL-6 production by macrophages is altered in response to LPS from periodontal bacteria, which may exacerbate IL-6-related systemic diseases caused by invading periodontal bacteria in patients with periodontal disease.