Department of Periodontology, School of Dentistry, Lille University Hospital, Lille, France.
EA SIMPA 7300, University of Lorraine, Nancy, France.
J Clin Periodontol. 2018 Jul;45(7):799-805. doi: 10.1111/jcpe.12925. Epub 2018 Jun 8.
Periodontal disease involves the activation of host immune response, acting not only as defender of periodontal tissues against bacterial aggression but also as mediator of tissue destruction. Triggering receptor expressed on myeloid cells 1 (TREM-1) is an immune receptor that synergizes with Toll-like receptors in amplifying the inflammatory response mediated by microbial molecules.
To investigate the role of P. gingivalis lipopolysaccharide (LPS) and the effect of LR12, a TREM-1 inhibitory peptide, on the expression of membrane-bound and soluble form of TREM-1 on human primary monocytes, as well as the production of proinflammatory cytokines.
Cells were stimulated with 1 μg/ml of LPS with or without LR12. PCR, flow cytometry and ELISA were used to determine TREM-1 expressions and cytokines release by monocytes.
P. gingivalis LPS can induce a significant increase in TREM-1 expression (mRNA, membrane-bound and soluble form, p < 0.001) as well as cytokines (IL-1β, TNFα) and chemokines (IL-8) production by monocytes. This monocytes' activation was partly prevented by LR12.
TREM-1 inhibitors such as LR12 could be interesting for the modulation of the excessive inflammatory response that occurs during periodontal disease.
研究牙龈卟啉单胞菌脂多糖（LPS）的作用，以及 TREM-1 抑制肽 LR12 对人原代单核细胞膜结合和可溶性形式的 TREM-1 表达以及促炎细胞因子产生的影响。
用 1μg/ml LPS 刺激细胞，有或没有 LR12。通过 PCR、流式细胞术和 ELISA 检测单核细胞中 TREM-1 的表达和细胞因子的释放。
牙龈卟啉单胞菌 LPS 可诱导单核细胞中 TREM-1 表达（mRNA、膜结合和可溶性形式，p<0.001）以及细胞因子（IL-1β、TNFα）和趋化因子（IL-8）的产生显著增加。LR12 部分阻止了这种单核细胞的激活。
TREM-1 抑制剂，如 LR12，可能对调节牙周病中发生的过度炎症反应具有重要意义。
