Willi M, Belibasakis G N, Bostanci N
Section of Oral Translational Research, Institute of Oral Biology, Center of Dental Medicine, University of Zürich, Zürich, Switzerland.
Clin Exp Immunol. 2014 Oct;178(1):190-200. doi: 10.1111/cei.12397.
Periodontitis is an inflammatory infectious disease that destroys the tooth-supporting tissues. It is caused by multi-species subgingival biofilms that colonize the tooth surface. Porphyromonas gingivalis, Treponema denticola and Tannerella forsythia (i.e. 'red complex' bacteria) are characteristic subgingival biofilm species. The triggering receptor expressed on myeloid cells 1 (TREM-1) is a cell surface receptor of the immunoglobulin superfamily, with a role in the amplification of proinflammatory cytokine production during infection. This study aimed to investigate TREM-1 mRNA expression in gingival tissues from patients with chronic periodontitis, generalized aggressive periodontitis and healthy subjects and its correlation with the levels of periodontal pathogens in the tissue. A further aim was to investigate the regulation of TREM-1 in human monocytic cells (MM6) challenged with an in-vitro subgingival biofilm model. Gingival tissue TREM-1 expression was increased in both chronic and aggressive periodontitis, compared to health, and correlated with the levels of the 'red complex' species in the tissue. No significant differences were detected between the two forms of periodontitis. Biofilm-challenged MM6 cells exhibited higher TREM-1 expression and secretion compared to controls, with partial involvement of the 'red complex'. Engagement or inhibition of TREM-1 affected the capacity of the biofilms to stimulate interleukin (IL)-1β, but not IL-8, secretion by the cells. In conclusion, this study reveals that TREM-1 tissue expression is enhanced in periodontal disease, and correlates with the level of periodontal pathogens. It also provides a mechanistic insight into the regulation of TREM-1 expression and the associated IL-1β production in biofilm-challenged monocytes.
牙周炎是一种破坏牙齿支持组织的炎症性感染性疾病。它由定植于牙齿表面的多种龈下生物膜引起。牙龈卟啉单胞菌、具核梭杆菌和福赛坦氏菌（即“红色复合体”细菌）是典型的龈下生物膜菌种。髓样细胞触发受体1（TREM-1）是免疫球蛋白超家族的一种细胞表面受体，在感染期间促炎细胞因子产生的放大过程中发挥作用。本研究旨在调查慢性牙周炎、广泛侵袭性牙周炎患者及健康受试者牙龈组织中TREM-1 mRNA的表达情况及其与组织中牙周病原体水平的相关性。另一个目的是研究在体外龈下生物膜模型刺激下，人单核细胞（MM6）中TREM-1的调控情况。与健康组相比，慢性和侵袭性牙周炎患者的牙龈组织TREM-1表达均增加，且与组织中“红色复合体”菌种的水平相关。两种形式的牙周炎之间未检测到显著差异。与对照组相比，受生物膜刺激的MM6细胞表现出更高的TREM-1表达和分泌，“红色复合体”部分参与其中。TREM-1的激活或抑制影响生物膜刺激细胞分泌白细胞介素（IL）-1β的能力，但不影响IL-8的分泌。总之，本研究表明牙周疾病中TREM-1组织表达增强，且与牙周病原体水平相关。它还为生物膜刺激的单核细胞中TREM-1表达的调控及相关IL-1β产生提供了机制性见解。
