論文 - 詳細
| RRC ID | 12458 |
|---|---|
| 著者 | Ara T, Kurata K, Hirai K, Uchihashi T, Uematsu T, Imamura Y, Furusawa K, Kurihara S, Wang PL. |
| タイトル | Human gingival fibroblasts are critical in sustaining inflammation in periodontal disease. |
| ジャーナル | J Periodontal Res |
| Abstract |
BACKGROUND AND OBJECTIVE:A major factor in the pathogenesis of periodontal disease, which is one of the biofilm infectious diseases, is thought to be lipopolysaccharide (LPS), owing to its ability to cause inflammation and promote tissue destruction. Moreover, the elimination of pathogens and their component LPSs is essential for the successful treatment of periodontal disease. Lipopolysaccharide tolerance is a mechanism that prevents excessive and prolonged responses of monocytes and macrophages to LPS. Since persistence of inflammation is necessary for inflammatory cytokine production, cells other than monocytes and macrophages are thought to maintain the production of cytokines in the presence of LPS. In this study, we investigated whether human gingival fibroblasts (HGFs), the most abundant structural cell in periodontal tissue, might be able to maintain inflammatory cytokine production in the presence of LPS bynot displaying LPS tolerance. MATERIAL AND METHODS:Human gingival fibroblasts were pretreated with LPS (from Porphyromonas gingivalis and Escherichia coli) and then treated with LPS, and the amounts of interleukin (IL)-6 and IL-8 in the cell culture supernatants were measured. The expression of negative regulators of LPS signalling (suppressor of cytokine signalling-1, interleukin-1 receptor-associated-kinase M and SH2 domain-containing inositol-5-phosphatase-1) was also examined in LPS-treated HGFs. RESULTS:Human gingival fibroblasts did not display LPS tolerance but maintained production of IL-6 and IL-8 when pretreated with LPS, followed by secondary LPS treatment. Lipopolysaccharide-treated HGFs did not express negative regulators. CONCLUSION:These results demonstrate that HGFs do not show LPS tolerance and suggest that this characteristic of HGFs sustains the inflammatory response in the presence of virulence factors. |
| 巻・号 | 44(1) |
| ページ | 21-7 |
| 公開日 | 2009-2-1 |
| DOI | 10.1111/j.1600-0765.2007.01041.x |
| PII | JRE1041 |
| PMID | 19515019 |
| MeSH | Actins / analysis Cell Line Cells, Cultured Escherichia coli / immunology Fibroblasts / immunology Fibroblasts / pathology* Gingiva / immunology Gingiva / pathology* Humans Immune Tolerance / immunology Inositol Polyphosphate 5-Phosphatases Interleukin-1 Receptor-Associated Kinases / analysis Interleukin-10 / pharmacology Interleukin-6 / analysis* Interleukin-8 / analysis* Lipopolysaccharides / immunology Periodontitis / immunology Periodontitis / pathology* Phosphoric Monoester Hydrolases / analysis Porphyromonas gingivalis / immunology Skin / immunology Skin / pathology Suppressor of Cytokine Signaling 1 Protein Suppressor of Cytokine Signaling Proteins / analysis Transforming Growth Factor beta1 / pharmacology src Homology Domains / immunology |
| IF | 2.926 |
| 引用数 | 103 |
| WOS 分野 | DENTISTRY, ORAL SURGERY & MEDICINE |
| リソース情報 | |
| ヒト・動物細胞 | THP-1(RCB1189) |