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目的:探究牙龈卟啉单胞菌（n Porphyromonas gingivalis，Pg）脂多糖（lipopolysaccharide，LPS）刺激巨噬细胞后，髓样细胞触发受体-1（triggering receptors expressed on myeloid cells-1，TREM-1）表达与M1、M2型极化的关系，进一步探讨巨噬细胞TREM-1在牙周炎发生发展中的作用机制。n 方法:使用豆蔻酰佛波醇乙酯诱导人单核细胞系THP-1分化为巨噬细胞，予以0（空白对照组）和1 μg/ml 的 Pg-LPS（LPS组）刺激，同期加入终质量浓度为0.1 μg/ml的TREM-1抑制剂LP17（LPS+LP17组）或对照肽（LPS+对照肽组），培养24 h后用实时荧光定量PCR（real-time quantitative-PCR，RT-qPCR）检测TREM-1和巨噬细胞M1、M2型极化标志物（分别为CD86、CD206）及其极化相关细胞因子［分别为肿瘤坏死因子-α（tumor necrosis factor-α，TNF-α）、白细胞介素（interleukin，IL）-1β、IL-10］mRNA表达变化，蛋白质印迹法检测TREM-1、CD86、CD206蛋白含量，酶联免疫吸附测定法检测巨噬细胞培养上清液中TNF-α、IL-1β及IL-10的表达。结果:细胞培养24 h后，LPS组巨噬细胞中TREM-1相对 mRNA表达量（1.40±0.14）及蛋白表达量（3.85±0.24）均较空白对照组（分别为1.01±0.18、1.00±0.05）显著升高（n P<0.05），同时M1型极化标志物CD86 mRNA及蛋白表达（分别为1.42±0.01、1.55±0.07）均较空白对照组（分别为1.00±0.09、1.00±0.10）显著上调（n P<0.01），且M1型极化相关细胞因子TNF-α、IL-1β mRNA及蛋白表达量均显著增加（n P0.05），CD86 mRNA（0.96±0.00）和蛋白（1.36±0.02）表达水平均显著下降（n P<0.05），TNF-α、IL-1β mRNA及蛋白表达水平均显著降低（n P<0.05）。对于M2型极化标志物CD206及极化相关细胞因子IL-10，细胞培养24 h后，CD206 mRNA（0.56±0.05）及蛋白表达（0.25±0.04）均较空白对照组（分别为1.02±0.25、1.00±0.10）显著下调（n P<0.01），IL-10 mRNA较空白对照组表达显著上调（n P0.05）；LPS+LP17组CD206、IL-10 mRNA表达均较LPS组显著下调（n P0.05）。n 结论:TREM-1及其下游信号通路可能参与了Pg-LPS介导的巨噬细胞M1型极化，从而在牙周炎发生发展中发挥促炎作用；尚无证据表明TREM-1是否参与调控Pg-LPS介导的巨噬细胞M2型极化。“,”Objective:To investigate the relationship between pattern recognition receptor triggering receptors expressed on myeloid cells-1 (TREM-1) and M1/M2 polarization in macrophages stimulated by n Porphyromonas gingivalis lipopolysaccharide (Pg-LPS), so as to explore the mechanism of TREM-1 in periodontitis.n Methods:Human monocytic cell line THP-1 were induced to differentiate into macrophages by phorbol-12-myristate-13-acetate and stimulated by 0 (blank control group) and 1 μg/ml Pg-LPS (LPS group), respectively. LP17, the TREM-1 inhibitor (LPS+LP17 group) and its control peptide (LPS+control peptide group) with final concentration of 0.1 μg/ml were added at the same time. After 24 hours stimulation, the expression of TREM-1, M1 markers and related cytokines [CD86, tumor necrosis factor-α (TNF-α), interleukin (IL)-1β], M2 markers and related cytokines (CD206,IL-10) mRNA were detected by real-time quantitative-PCR (RT-qPCR), the level of TREM-1, CD86 and CD206 proteins were detected by Western blotting, and TNF-α, IL-1β and IL-10 in the macrophage culture supernatant were detected by enzyme linked immunosorbent assay.Results:After 24 h of cell culture, the relative expressions of TREM-1 mRNA (1.40±0.14) and protein (3.85±0.24) in macrophages in the LPS group increased compared with the blank control group (1.01±0.18 and 1.00±0.05, respectively) (n P<0.05). Meanwhile, the expression levels of M1 markers CD86 mRNA and protein [LPS group vs blank control group were (1.42±0.01 vs 1.00±0.09) and (1.55±0.07 vs 1.00±0.10), respectively] were up-regulated (n P<0.01), and the expressions of mRNA and protein of M1 related cytokines TNF-α and IL-1 increased (n P0.05), while the levels of CD86 mRNA (0.96±0.00) and protein (1.36±0.02) decreased (n P<0.05), and the levels of TNF-α and IL-1 further decreased (n P<0.05). For M2 marker CD206 and related cytokine IL-10, CD206 mRNA (0.56±0.05) and protein (0.25±0.04) were significantly down-regulated (n P<0.01) compared with the blank control group (1.02±0.25 and 1.00±0.10, respectively), and IL-10 mRNA was up-regulated compared with the blank control group (n P0.05). After the addition of LP17, the expressions of CD206 and IL-10 mRNA in the LPS+LP17 group were further down-regulated compared with the LPS group (n P0.05).n Conclusions:TREM-1 and its downstream signaling pathway might be involved in M1 polarization of Pg-LPS-mediated macrophages, thus playing a pro-inflammatory role in the development of periodontitis. There is no obvious evidence that TREM-1 is involved in regulating M2 polarization of Pg-LPS-mediated macrophages.