Effects of Porphyromonas gingivalis LPS and LR12 peptide on TREM‐1 expression by monocytes
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‐l...
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Published in | Journal of clinical periodontology Vol. 45; no. 7; pp. 799 - 805 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
United States
Blackwell Publishing Ltd
01.07.2018
Wiley |
Subjects | |
Online Access | Get full text |
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Summary: | 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 LR12, 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 LR12. 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, TNFα) and chemokines (IL‐8) production by monocytes. This monocytes’ activation was partly prevented by LR12.
Conclusions
TREM‐1 inhibitors such as LR12 could be interesting for the modulation of the excessive inflammatory response that occurs during periodontal disease. |
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Bibliography: | Funding information This study was supported by the Association CONCEPT PARODONTAL. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0303-6979 1600-051X |
DOI: | 10.1111/jcpe.12925 |