title: Activation of the TREM-1 pathway in human monocytes by periodontal pathogens and oral commensal bacteria.
abstract: Periodontitis is a highly prevalent disease caused in part by an aberrant host response to the oral multi-species biofilm. A balance between the oral bacteria and host immunity is essential for oral health. Imbalances in the oral microbiome lead to an uncontrolled host inflammatory response and subsequent periodontal disease (i.e. gingivitis and periodontitis). TREM-1 is a signaling receptor present on myeloid cells capable of acting synergistically with other pattern recognition receptors leading to amplification of inflammatory responses. The aim of this study was to investigate the activation of the TREM-1 pathway in the human monocyte-like cell line THP-1 exposed to both oral pathogens and commensals. The relative expression of the genes encoding TREM-1 and its adapter protein DAP12 were determined by quantitative real-time polymerase chain reaction. The surface expression of TREM-1 was determined by flow cytometry. Soluble TREM-1 and cytokines were measured by enzyme-linked immunosorbent assay. The results demonstrate that both commensal and pathogenic oral bacteria activate the TREM-1 pathway, resulting in a proinflammatory TREM-1 activity-dependent increase in proinflammatory cytokine production.
authors.affiliation: Department of Oral Biology, University at Buffalo, School of Dental Medicine, State University of New York, Buffalo, NY, USA.
authors.forename: M
authors.initials: M
authors.lastname: Varanat
authors.affiliation: Department of Oral Biology, University at Buffalo, School of Dental Medicine, State University of New York, Buffalo, NY, USA.
authors.forename: E M
authors.initials: EM
authors.lastname: Haase
authors.affiliation: Department of Oral Biology, University at Buffalo, School of Dental Medicine, State University of New York, Buffalo, NY, USA.
authors.forename: J G
authors.initials: JG
authors.lastname: Kay
authors.affiliation: Department of Oral Biology, University at Buffalo, School of Dental Medicine, State University of New York, Buffalo, NY, USA.
authors.forename: F A
authors.initials: FA
authors.lastname: Scannapieco
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000235:genetics / Q000378:metabolism; D001419:Bacteria / Q000276:immunology* / Q000472:pathogenicity*; D002478:Cells, Cultured; D016207:Cytokines / Q000235:genetics; D005434:Flow Cytometry; D006801:Humans; D007113:Immunity, Innate; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism; D009000:Monocytes / Q000382:microbiology*; D010510:Periodontal Diseases / Q000276:immunology* / Q000382:microbiology; D016966:Porphyromonas gingivalis / Q000276:immunology / Q000472:pathogenicity; D060888:Real-Time Polymerase Chain Reaction; D015398:Signal Transduction; D054773:Streptococcus gordonii / Q000276:immunology / Q000472:pathogenicity; D013559:Symbiosis; D000074084:THP-1 Cells; D000073871:Triggering Receptor Expressed on Myeloid Cells-1 / Q000235:genetics / Q000378:metabolism*
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D016207:Cytokines; D008565:Membrane Proteins; C110546:TYROBP protein, human; D000073871:Triggering Receptor Expressed on Myeloid Cells-1
keywords: 
  Porphyromonas
  ; 
  Streptococcus
  ; cell receptors; innate immunity; mucosal immune responses; periodontal disease