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首页> 外文期刊>Journal of periodontal research >Expression of suppressors of cytokine signaling in diseased periodontal tissues: a stop signal for disease progression?
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Expression of suppressors of cytokine signaling in diseased periodontal tissues: a stop signal for disease progression?

机译:病变牙周组织中细胞因子信号转导抑制剂的表达:疾病进展的终止信号?

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摘要

BACKGROUND AND OBJECTIVE: Inflammatory cytokines are thought to trigger periodontal tissue destruction. In addition to being regulated by anti-inflammatory mediators, their activity is under the control of suppressors of cytokine signaling (SOCS), which down-regulate the signal transduction as part of an inhibitory feedback loop. We therefore investigated the expression of SOCS-1, -2 and -3, and the cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-10, in different forms of human periodontal diseases. MATERIAL AND METHODS: Quantitative polymerase chain reaction (RealTime-PCR) was performed with mRNA from gingival biopsies of control subjects and from that of patients with chronic gingivitis and chronic periodontitis. RESULTS: Our results show that patients with chronic gingivitis and chronic periodontitis exhibit significantly higher SOCS-1, -2 and -3, TNF-alpha and interleukin-10 mRNA expression when compared with healthy controls. The data also demonstrate that SOCS-1 and -3 mRNA expression was higher in tissue from patients with chronic gingivitis than chronic periodontitis, while the levels of SOCS-2, TNF-alpha and interleukin-10 mRNA were similar in these groups. CONCLUSION: The increased expression of SOCS-1, -2 and -3 mRNA in diseased periodontal tissues is believed to be involved in the down-regulation of inflammatory cytokine and Toll-like receptor signaling, and therefore in the attenuation of both the inflammatory reaction and disease severity. Furthermore, it is possible that variation in the levels of SOCS mRNA expressed in different forms of periodontal diseases may determine the stable or progressive nature of the lesions.
机译:背景与目的:炎症细胞因子被认为可引起牙周组织破坏。除了受到抗炎介质的调节外,它们的活性还受细胞因子信号传导抑制因子(SOCS)的控制,后者抑制信号转导,成为抑制性反馈回路的一部分。因此,我们研究了SOCS-1,-2和-3以及细胞因子肿瘤坏死因子-α(TNF-alpha)和白细胞介素10在不同形式的人类牙周疾病中的表达。材料与方法:定量聚合酶链反应(RealTime-PCR)用来自对照对象以及慢性牙龈炎和慢性牙周炎患者的牙龈活检的mRNA进行。结果:我们的结果表明,与健康对照相比,患有慢性牙龈炎和慢性牙周炎的患者的SOCS-1,-2和-3,TNF-α和白介素10 mRNA表达明显更高。数据还表明,慢性牙龈炎患者组织中SOCS-1和-3 mRNA的表达高于慢性牙周炎,而这些组中SOCS-2,TNF-α和白细胞介素10 mRNA的水平相似。结论:患牙周组织中SOCS-1,-2和-3 mRNA的表达增加被认为与炎性​​细胞因子和Toll样受体信号转导的下调有关,因此与炎症反应的减弱有关。和疾病的严重程度。此外,以不同形式的牙周疾病表达的SOCS mRNA水平的变化可能会决定病变的稳定或进行性。

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