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Effects of Porphyromonas gingivalis LPS and LR 12 peptide on TREM ‐1 expression by monocytes
Author(s) -
Dubar Marie,
Carrasco Kevin,
Gibot Sebastien,
Bisson Catherine
Publication year - 2018
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/jcpe.12925
Subject(s) - porphyromonas gingivalis , proinflammatory cytokine , chemokine , lipopolysaccharide , immune system , receptor , chemistry , flow cytometry , monocyte , immunology , inflammation , microbiology and biotechnology , biology , bacteria , biochemistry , genetics
Periodontal disease involves the activation of host immune response, acting not only as defender of periodontal tissues against bacterial aggression but also as mediator of tissue destruction. Triggering receptor expressed on myeloid cells 1 ( TREM ‐1) is an immune receptor that synergizes with Toll‐like receptors in amplifying the inflammatory response mediated by microbial molecules. Aim To investigate the role of P. gingivalis lipopolysaccharide ( LPS ) and the effect of LR 12, a TREM ‐1 inhibitory peptide, on the expression of membrane‐bound and soluble form of TREM ‐1 on human primary monocytes, as well as the production of proinflammatory cytokines. Material and Methods Cells were stimulated with 1 μg/ml of LPS with or without LR 12. PCR , flow cytometry and ELISA were used to determine TREM ‐1 expressions and cytokines release by monocytes. Results P. gingivalis LPS can induce a significant increase in TREM ‐1 expression ( mRNA , membrane‐bound and soluble form, p < 0.001) as well as cytokines ( IL ‐1β, TNF α) and chemokines ( IL ‐8) production by monocytes. This monocytes’ activation was partly prevented by LR 12. Conclusions TREM ‐1 inhibitors such as LR 12 could be interesting for the modulation of the excessive inflammatory response that occurs during periodontal disease.