[Porphyromonas gingivalis lipopolysaccharide regulates macrophage polarization via triggering receptors expressed on myeloid cells-1].

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 Porphyromonas gingivalis lipopolysaccharide (Pg-LPS), so as to explore the mechanism of TREM-1 in periodontitis. 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) (P 0.05), while the levels of CD86 mRNA (0.96±0.00) and protein (1.36±0.02) decreased (P 0.05). 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 (P 0.05). 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.