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Effect of interleukin-17A on inflammatory mediator production in interleukin-1β-stimulated human dental pulp fibroblasts

https://tokushima-u.repo.nii.ac.jp/records/2012489
https://tokushima-u.repo.nii.ac.jp/records/2012489
eb2bd2c8-9f2e-42eb-b48d-7c59a502c0dc
名前 / ファイル ライセンス アクション
eos_132_5_e13019.pdf eos_132_5_e13019.pdf (902 KB)
アイテムタイプ 文献 / Documents(1)
公開日 2025-02-26
アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
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
出版社版DOI
関連識別子 https://doi.org/10.1111/eos.13019
関連名称 10.1111/eos.13019
出版タイプ
出版タイプ AM
出版タイプResource http://purl.org/coar/version/c_ab4af688f83e57aa
タイトル
タイトル Effect of interleukin-17A on inflammatory mediator production in interleukin-1β-stimulated human dental pulp fibroblasts
タイトル別表記
その他のタイトル Effect of IL-17A on dental pulp cells
著者 中西, 正

× 中西, 正

WEKO 1704
徳島大学 教育研究者総覧 60419/profile-ja.html
e-Rad_Researcher 00217770

ja 中西, 正
中西, 正
ISNI

ja-Kana ナカニシ, タダシ
ナカニシ, タダシ

en Nakanishi, Tadashi
Nakanishi, Tadashi

Search repository
Mieda, Katsuhiro

× Mieda, Katsuhiro

en Mieda, Katsuhiro

Search repository
Kuramoto, Hitomi

× Kuramoto, Hitomi

en Kuramoto, Hitomi

Search repository
武川, 大輔

× 武川, 大輔

WEKO 566
徳島大学 教育研究者総覧 246736/profile-ja.html
e-Rad_Researcher 10632664

ja 武川, 大輔
武川, 大輔
ISNI

ja-Kana タケガワ, ダイスケ
タケガワ, ダイスケ

en Takegawa, Daisuke
Takegawa, Daisuke

Search repository
抄録
内容記述 In response to pro-inflammatory cytokines such as interleukin (IL)-1β, dental pulp fibroblasts produce various inflammatory mediators, including IL-6, IL-8, CC chemokine ligand 20 (CCL20) and CXC chemokine ligand 10 (CXCL10), leading to the progression of pulpitis. IL-17/IL-17A (IL-17A) is a pro-inflammatory cytokine secreted by T helper (Th) 17 cells following their recruitment to inflamed sites; however, the roles of IL-17A during pulpitis remain unclear. The purpose of this study was to investigate the effect of IL-17A on IL-6, IL-8, CCL20 and CXCL10 production by human dental pulp fibroblasts (HDPFs) in vitro. IL-17A at a concentration of 100 ng/ml induced the production of 10 times more IL-8 and 4 times more CXCL10, but not IL-6 and CCL20, compared to controls. Co-stimulation of HDPFs with IL-17A and IL-1β synergistically enhanced the production of IL-6, CCL20, IL-8 and CXCL10. IL-1β increased expression of IL-17 receptor/IL-17RA (IL-17R) on HDPFs. Moreover, the cell signal pathways of p38 mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) were more potently activated by simultaneous stimulation with IL-17A and IL-1β. These findings suggest that IL-17A participates in the progression of dental pulp inflammation through the enhanced production of inflammatory mediators in HDPFs.
キーワード
主題 chemokines
キーワード
主題 cytokines
キーワード
主題 endodontics
キーワード
主題 pulpitis
書誌情報 en : European Journal of Oral Sciences

巻 132, 号 5, p. e13019, 発行日 2024-09-20
収録物ID
収録物識別子タイプ EISSN
収録物識別子 16000722
収録物ID
収録物識別子タイプ PISSN
収録物識別子 09098836
収録物ID
収録物識別子タイプ NCID
収録物識別子 AA11623000
収録物ID
収録物識別子タイプ NCID
収録物識別子 AA11033550
出版者
出版者 John Wiley & Sons Ltd
備考
値 This is the peer reviewed version of the following article: Nakanishi, T., Mieda, K., Kuramoto, H., Takegawa, D. (2024), Effect of interleukin-17A on inflammatory mediator production in interleukin-1β-stimulated human dental pulp fibroblasts. European Journal of Oral Sciences, 132, 5, e13019., which has been published in final form at https://doi.org/10.1111/eos.13019. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions. This article may not be enhanced, enriched or otherwise transformed into a derivative work, without express permission from Wiley or by statutory rights under applicable legislation. Copyright notices must not be removed, obscured or modified. The article must be linked to Wiley’s version of record on Wiley Online Library and any embedding, framing or otherwise making available the article or pages thereof by third parties from platforms, services and websites other than Wiley Online Library must be prohibited.
EID
識別子 416188
言語
言語 eng
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