The browser you are using is not supported by this website. All versions of Internet Explorer are no longer supported, either by us or Microsoft (read more here: https://www.microsoft.com/en-us/microsoft-365/windows/end-of-ie-support).

Please use a modern browser to fully experience our website, such as the newest versions of Edge, Chrome, Firefox or Safari etc.

Differential effects of LPS from Escherichia coli and Porphyromonas gingivalis on IL-6 production in human periodontal ligament cells.

Author

Summary, in English

Abstract Objective. Periodontal ligament (PDL) cells produce IL-6 upon stimulation with inflammation promoters, but the signaling pathways involved have not been characterized. This study investigates underlying mechanisms behind regulation of PDL cell IL-6 production by E. coli and P. gingivalis LPS. Materials and methods: Human PDL cells, endothelial cells and monocytes were stimulated with E. coli or P. gingivalis LPS in the presence or absence of pharmacological agents in order to disclose pathways involved in LPS signaling. Gene expression and cellular protein levels were assessed by quantitative real-time PCR and ELISA, respectively. Results. Stimulation with LPS from E. coli (1 µg/ml) for 24 h enhanced PDL cell IL-6 expression several fold, demonstrated both on transcript and protein levels, but P. gingivalis LPS (1-5 µg/ml) had no effect. TLR2 mRNA was more highly expressed than TLR4 transcript in PDL cells. Treatment with the non-selective nitric oxide synthase inhibitor L-NAME (100 µM) reduced E. coli LPS-induced PDL cell IL-6 by 30%, while neither aminoguanidine (10 µM), an inhibitor of inducible nitric oxide synthase, nor estrogen (17β-estradiol, 100 nM) influenced IL-6. Treatment with the glucocorticoid dexamethasone (1 µM) totally prevented the E. coli LPS-induced PDL cell IL-6. In endothelial cells, neither E. coli LPS nor P. gingivalis LPS promoted IL-6 production. In monocytes, serving as positive control, both E. coli and P. gingivalis LPS stimulated IL-6. Conclusions. E. coli LPS but not P. gingivalis LPS stimulates PDL cell IL-6 production through a glucocorticoid-sensitive mechanism involving nitric oxide formation, probably via endothelial nitric oxide synthase.

Publishing year

2013

Language

English

Pages

892-898

Publication/Series

Acta Odontologica Scandinavica

Volume

71

Issue

3-4

Document type

Journal article

Publisher

Taylor & Francis

Topic

  • Dentistry

Status

Published

Project

  • Regulation of pro-inflammatory cytokine expression in periodontal ligament cells

Research group

  • Vascular Physiology

ISBN/ISSN/Other

  • ISSN: 1502-3850