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Interleukin (IL)-6, IL-8, and the chemical mediator\nprostaglandin E2 (PGE2) are known to play important roles in inflammatory responses and tissue degradation.\nRecently, we reported that the protein kinase A (PKA) inhibitor H-89 suppresses lipopolysaccharide (LPS)-induced\nIL-8 production by human gingival fibroblasts (HGFs). In the present study, the relevance of the PKA activity and\ntwo PKA-activating drugs, aminophylline and adrenaline, to LPS-induced inflammatory cytokines (IL-6 and IL-8) and\nPGE2 by HGFs were examined.\nMethods: HGFs were treated with LPS from Porphyromonas gingivalis and H-89, the cAMP analog dibutyryl cyclic\nAMP (dbcAMP), aminophylline, or adrenaline. After 24 h, IL-6, IL-8, and PGE2 levels were evaluated by ELISA.\nResults: H-89 did not affect LPS-induced IL-6 production, but suppressed IL-8 and PGE2 production. In contrast,\ndbcAMP significantly increased LPS-induced IL-6, IL-8, and PGE2 production. Up to 10 μg/ml of aminophylline did\nnot affect LPS-induced IL-6, IL-8, or PGE2 production, but they were significantly increased at 100 μg/ml. Similarly,\n0.01 μg/ml of adrenaline did not affect LPS-induced IL-6, IL-8, or PGE2 production, but they were significantly\nincreased at concentrations of 0.1 and 1 μg/ml. In the absence of LPS, H-89, dbcAMP, aminophylline, and\nadrenaline had no relevance to IL-6, IL-8, or PGE2 production.\nConclusion: These results suggest that the PKA pathway, and also PKA-activating drugs, enhance LPS-induced IL-6,\nIL-8, and PGE2 production by HGFs. However, aminophylline may not have an effect on the production of these\nmolecules at concentrations used in clinical settings (8 to 20 μg/ml in serum). 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Protein kinase A enhances lipopolysaccharideinduced IL-6, IL-8, and PGE2 production by human gingival broblasts
https://mdu.repo.nii.ac.jp/records/2282
https://mdu.repo.nii.ac.jp/records/22823e096a51-404d-4350-8618-5fd3db759342
名前 / ファイル | ライセンス | アクション |
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Item type | 松本歯学/学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2014-10-06 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | Protein kinase A enhances lipopolysaccharideinduced IL-6, IL-8, and PGE2 production by human gingival broblasts | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Protein kinase A | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | interleukin, | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | prostaglandin E2 | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | human gingival fibroblast | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Cyclic AMP-Dependent Protein Kinases | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Dinoprostone | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Fibroblasts | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Gingiva | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Interleukin-6 | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Interleukin-8 | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | Lipopolysaccharides | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者 |
ARA, TOSHIAKI
× ARA, TOSHIAKI× FUJINAMI, YOSHIAKI× URANO, HIROKO× HIRAI, KANAME× HATTORI, TOSHIMI× MIYAZAWA, HIROO |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Objective: Periodontal disease is accompanied by inflammation of the gingiva and destruction of periodontal tissues, leading to alveolar bone loss in severe clinical cases. Interleukin (IL)-6, IL-8, and the chemical mediator prostaglandin E2 (PGE2) are known to play important roles in inflammatory responses and tissue degradation. Recently, we reported that the protein kinase A (PKA) inhibitor H-89 suppresses lipopolysaccharide (LPS)-induced IL-8 production by human gingival fibroblasts (HGFs). In the present study, the relevance of the PKA activity and two PKA-activating drugs, aminophylline and adrenaline, to LPS-induced inflammatory cytokines (IL-6 and IL-8) and PGE2 by HGFs were examined. Methods: HGFs were treated with LPS from Porphyromonas gingivalis and H-89, the cAMP analog dibutyryl cyclic AMP (dbcAMP), aminophylline, or adrenaline. After 24 h, IL-6, IL-8, and PGE2 levels were evaluated by ELISA. Results: H-89 did not affect LPS-induced IL-6 production, but suppressed IL-8 and PGE2 production. In contrast, dbcAMP significantly increased LPS-induced IL-6, IL-8, and PGE2 production. Up to 10 μg/ml of aminophylline did not affect LPS-induced IL-6, IL-8, or PGE2 production, but they were significantly increased at 100 μg/ml. Similarly, 0.01 μg/ml of adrenaline did not affect LPS-induced IL-6, IL-8, or PGE2 production, but they were significantly increased at concentrations of 0.1 and 1 μg/ml. In the absence of LPS, H-89, dbcAMP, aminophylline, and adrenaline had no relevance to IL-6, IL-8, or PGE2 production. Conclusion: These results suggest that the PKA pathway, and also PKA-activating drugs, enhance LPS-induced IL-6, IL-8, and PGE2 production by HGFs. However, aminophylline may not have an effect on the production of these molecules at concentrations used in clinical settings (8 to 20 μg/ml in serum). These results suggest that aminophylline does not affect inflammatory responses in periodontal disease. |
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書誌情報 |
en : Journal of Negative Results in BioMedicine 巻 10, p. 11, 発行日 2012 |
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出版者 | ||||||
出版者 | BioMed Central | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 1477-5751 | |||||
PubMed番号 | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | PMID | |||||
関連識別子 | info:pmid/22452847 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | https://doi.org/10.1186/1477-5751-11-10. | |||||
関連名称 | info:doi/10.1186/1477-5751-11-10. | |||||
権利 | ||||||
権利情報 | © 2012 Ara et al; licensee BioMed Central Ltd. | |||||
情報源 | ||||||
関連名称 | 雑誌掲載論文(電子版) | |||||
関連サイト | ||||||
識別子タイプ | URI | |||||
関連識別子 | http://www.jnrbm.com/content/11/1/10 | |||||
関連名称 | BioMed Central Ltd | |||||
フォーマット | ||||||
内容記述タイプ | Other | |||||
内容記述 | application/pdf | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 |