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细胞因子在培养的人牙龈成纤维细胞上诱导黏附分子的作用。

Role of cytokine in the induction of adhesion molecules on cultured human gingival fibroblasts.

作者信息

Takahashi K, Takigawa M, Takashiba S, Nagai A, Miyamoto M, Kurihara H, Murayama Y

机构信息

Department of Periodontology and Endodontology, Okayama University Dental School, Japan.

出版信息

J Periodontol. 1994 Mar;65(3):230-5. doi: 10.1902/jop.1994.65.3.230.

Abstract

This study was undertaken in an effort to understand the role of cytokines on human gingival fibroblasts and T lymphocyte trafficking into inflamed gingival tissue. Using flow cytometry we examined gingival fibroblasts to determine the level of cell surface expression and the percentage of cells positive for intercellular adhesion molecule 1 (ICAM-1), the HLA-DR antigen, lymphocyte function-associated antigen 3 (LFA-3), and the CD44 molecule, which are involved in antigen presentation. The following cytokines were used: interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), IL-6, and IL-8. The levels of ICAM-1 expression were enhanced in a dose- and time-dependent manner by IL-1 beta, TNF-alpha, or IFN-gamma, but not by IL-6 or IL-8. HLA-DR surface expression was induced only by IFN-gamma in a dose- and time-dependent manner, but not by the other cytokines tested. In contrast, the expression of LFA-3 and the CD44 molecule could be detected without the stimulation of any cytokine, but the levels of their expression were not significantly changed by any cytokines. The enhanced ICAM-1 expression by cytokines was reduced in a time-dependent manner following the removal of cytokines from the reaction mixture, while IFN-gamma-induced HLA-DR expression was maintained even 7 days after the removal of IFN-gamma. These data support an interactive role for inflammatory cytokines and the expression of adhesion molecules on gingival fibroblasts in the pathogenesis of gingival inflammation in periodontal disease.

摘要

本研究旨在了解细胞因子在人牙龈成纤维细胞以及T淋巴细胞向炎症牙龈组织迁移中的作用。我们使用流式细胞术检测牙龈成纤维细胞,以确定细胞表面表达水平以及细胞间黏附分子1(ICAM-1)、HLA-DR抗原、淋巴细胞功能相关抗原3(LFA-3)和CD44分子阳性细胞的百分比,这些分子均参与抗原呈递。使用了以下细胞因子:白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)、干扰素-γ(IFN-γ)、IL-6和IL-8。IL-1β、TNF-α或IFN-γ可使ICAM-1表达水平呈剂量和时间依赖性增强,而IL-6或IL-8则无此作用。仅IFN-γ可使HLA-DR表面表达呈剂量和时间依赖性诱导,而其他受试细胞因子则无此作用。相反,在未受到任何细胞因子刺激的情况下即可检测到LFA-3和CD44分子的表达,但其表达水平不会因任何细胞因子而发生显著变化。从反应混合物中去除细胞因子后,细胞因子诱导的ICAM-1表达增强以时间依赖性方式降低,而IFN-γ诱导的HLA-DR表达即使在去除IFN-γ 7天后仍维持。这些数据支持炎症细胞因子与牙龈成纤维细胞上黏附分子表达在牙周病牙龈炎症发病机制中具有相互作用。

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