徳島大学 教育・研究者情報データベース(EDB)

1. 木戸 淳一

   役割	任意
   貢献度	任意
   学籍番号	推奨

2. (英) Kido Reiko

   役割	任意
   貢献度	任意
   学籍番号	推奨

3. (英) Suryono

   役割	任意
   貢献度	任意
   学籍番号	推奨

4. 片岡 正俊

   役割	任意
   貢献度	任意
   学籍番号	推奨

5. (英) Fagerhol K. Magne

   役割	任意
   貢献度	任意
   学籍番号	推奨

6. 永田 俊彦

   役割	任意
   貢献度	任意
   学籍番号	推奨

(英) Calprotectin release from human neutrophils is induced by Porphyromonas gingivalis lipopolysaccharide via the CD-14-Toll-like receptor-nuclear factor kB pathway

(英) Calprotectin is a cytosolic protein with antibacterial action in leukocytes and its level increases in some inflammatory diseases, including periodontal diseases, rheumatoid arthritis and ulcerative colitis. Recently, we found that the lipopolysaccharide of Porphyromonas gingivalis (P-LPS) induced calprotectin release from human neutrophils. P-LPS, a major virulence factor of periodontal pathogens, is known to induce the production and release of inflammatory cytokines through CD14, Toll-like receptor (TLR) and nuclear factor kappaB (NF-kappaB). In the present study, we investigated whether calprotectin release by P-LPS is induced via the CD14-TLR-NF-kappaB pathway and the cellular mechanism of calprotectin release in human neutrophils. Human neutrophils were isolated from the peripheral blood of healthy donors and pre-incubated in medium containing antibodies against CD14, TLR2 and TLR4, or several inhibitors of NF-kappaB, microtubules and microfilaments, and then incubated with P-LPS. The calprotectin amount in the culture medium was determined using ELISA, and the nuclear extracts from cells were used for the examination of NF-kappaB binding activity using electrophoretic mobility shift assays. P-LPS increased calprotectin release from neutrophils and its induction was inhibited by anti-CD14 and anti-TLR2 antibodies, but not by two anti-TLR4 antibodies. NF-kappaB inhibitors suppressed P-LPS-induced NF-kappaB binding activity and calprotectin release. The inhibitors of microtubule and microfilament polymerization significantly decreased P-LPS-induced calprotectin release. These results suggest that calprotectin release is induced by P-LPS via the CD14-TLR2-NF-kappaB signal pathway in human neutrophils and may be dependent on microtubule and microfilament systems.

1. (英) calprotectin
2. (英) Porphyromonas gingivalis
3. (英) lipopolysaccharide

1. (英) Article.Affiliation: Department of Periodontology and Endodontology, Tokushima University School of Dentistry, Kuramoto, Tokushima, Japan. kido@dent.tokushima-u.ac.jp

2. (英) Article.PublicationTypeList.PublicationType: Journal Article

3. (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't