口腔医学研究 ›› 2015, Vol. 31 ›› Issue (3): 213-216.

• 基础研究论著 • 上一篇    下一篇

牙龈卟啉单胞菌脂多糖对髓系细胞触发受体的激活作用

洪菲菲1, 雷浪2, 潘盛波2, 李厚轩3*, 闫福华3*   

  1. 1. 厦门市口腔医院牙周科 福建 厦门 361003;
    2. 福建医科大学附属口腔医院·口腔医学院,福建省高校口腔医学重点实验室;
    3. 南京大学医学院附属口腔医院
  • 收稿日期:2014-07-31 出版日期:2015-03-28 发布日期:2016-04-29
  • 通讯作者: 李厚轩,E-mail: lihouxuan3435_0@163.com
    闫福华,E-mail: fhyan2005@126.com
  • 作者简介:洪菲菲(1988~ ),女,福建南平人,硕士,医师,主要从事牙周病和全身疾病关系的研究。
  • 基金资助:
    国家自然科学基金资助项目(编号:81400516、81170973、81100760)

Activation of Triggering Receptor Expressed on Myeloid Cells by Lipopolysacchride from Porphyromonas Gingivalis.

HONG Fei-fei, LEI Lang, PAN Sheng-bo, et al.   

  1. Department of Periodontology, Xiamen Stomatological Hospital, Xiameng 3610032
  • Received:2014-07-31 Online:2015-03-28 Published:2016-04-29

摘要: 目的:研究牙龈卟啉单胞菌(Pg)脂多糖(LPS)对巨噬细胞中髓系细胞触发受体-1(TREM-1)和-2的激活作用。方法:分离培养小鼠腹腔巨噬细胞,并以1 mg/L的Pg-LPS刺激。采用实时荧光定量PCR技术检测TLR-2、TLR-4、TREM-1和TREM-2转录水平的变化,流式细胞术检测蛋白水平的变化,酶联免疫反应检测培养液中肿瘤坏死因子-α(TNF-α)和巨噬细胞炎症蛋白-lα(MIP-lα)水平的变化。 结果:Pg-LPS刺激巨噬细胞2 h后,巨噬细胞内TLR-2和TREM-1的转录水平均表达上调;流式细胞检测显示24 h后,细胞内TREM-1和TLR-2水平显著上调;TLR-4和TREM-2在实验中未见显著变化;Pg-LPS刺激巨噬细胞24 h后,TNF-α和MIP-1α水平显著上升组;TREM-1的抑制物LP-17多肽显著抑制了Pg-LPS的炎症刺激作用。结论:TLR-2和TREM-1参与了巨噬细胞应答Pg-LPS的先天免疫过程。

关键词: 牙龈卟啉单胞菌, 脂多糖, 髓系细胞触发受体

Abstract: Objective: To investigate whether porphyromonas gingivalis lipopolysacchride(Pg-LPS) can activate triggering receptor expressed on myeloid cells to stimulate inflammatory response. Methods: Mice peritoneal macrophages were separated and cultured, then treated with Pg-LPS. Quantitative real time PCR was utilized to detect mRNA transcription of TLR-2, TLR-4, TREM-1 and TREM-2, and flow cytometry was used to quantify protein expression,and tumor necrosis factor-α(TNF-α) and macrophage inflammatory protein-1α(MIP-lα) in supernatants were detected by enzyme linked absorbent analysis (ELISA). Results: 2 h after Pg-LPS incubation, TLR-2 and TREM-1 mRNA transcription was up-regulated; 24 h after Pg-LPS treatment, increased TLR-2 and TREM-1 protein expression was detected; Pg-LPS did not significantly activate TLR-4 and TREM-2;Pg-LPS triggered TNF-α and MIP-lα release into cell culture. LP-17 polypeptide, an inhibitor of TREM-1, inhibited Pg-LPS stimulated cytokine production. Conclusion: TLR-2 and TREM-1 were involved in innate immune response to Pg-LPS.

Key words: Porphyromonas gingivalis , Polyliposacchride, Triggering receptor expressed on myeloid cells

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