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Activation of the TREM ‐1 pathway in human monocytes by periodontal pathogens and oral commensal bacteria
Author(s) -
Varanat M.,
Haase E.M.,
Kay J.G.,
Scannapieco F.A.
Publication year - 2017
Publication title -
molecular oral microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.18
H-Index - 77
eISSN - 2041-1014
pISSN - 2041-1006
DOI - 10.1111/omi.12169
Subject(s) - proinflammatory cytokine , porphyromonas gingivalis , microbiology and biotechnology , biology , oral microbiome , periodontitis , immunology , receptor , innate immune system , bacteria , immune system , microbiome , inflammation , medicine , biochemistry , genetics
Summary 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 DAP 12 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.