Open AccessDoxycycline inhibits TREM ‐1 induction by P orphyromonas gingivalis
Author(s) -
Bostanci Nagihan,
Belibasakis Georgios N.
Publication year - 2012
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2012.00982.x
Subject(s) - porphyromonas gingivalis , doxycycline , inflammation , secretion , cytokine , biology , receptor , periodontal pathogen , immunology , interleukin 6 , microbiology and biotechnology , pharmacology , periodontitis , medicine , endocrinology , antibiotics , biochemistry
The triggering receptor expressed on myeloid cells 1 ( TREM ‐1) is a cell surface receptor of the immunoglobulin superfamily, with the capacity to amplify pro‐inflammatory cytokine production. P orphyromonas gingivalis is a G ram‐negative anaerobic species highly implicated in inflammatory periodontal disease, with potential involvement in systemic inflammation. P orphyromonas gingivalis positively regulates TREM ‐1 expression and production in monocytic cells. Subantimicrobial doses of doxycycline ( SDD ) are used as an adjunct treatment in periodontal therapy, because of their anti‐inflammatory properties. The aim of this study was to investigate the effect of SDD on P . gingivalis ‐induced TREM ‐1 expression and secretion by the myelomonocytic cell line M ono M ac‐6. After 24 h of challenge, P . gingivalis enhanced TREM ‐1 gene expression by the cells, with a concomitant increase in soluble TREM ‐1 release. Nevertheless, SDD concentrations between 2 and 10 μg mL −1 abolished TREM ‐1 expression and release, already after 4 h of administration. Moreover, SDD reduced P . gingivalis ‐induced interleukin‐8 secretion, confirming its anti‐inflammatory effects. In conclusion, SDD inhibits bacterially induced TREM ‐1, and this effect may partly account for its generalized anti‐inflammatory properties. This could partly explain the clinical efficacy of SDD as an adjunctive treatment for periodontal disease, but may also indicate that SDD could serve as a suitable modulator of systemic inflammatory responses.