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LPS-induced MCP-1 and IL-6 production is not reversed by oestrogen in human periodontal ligament cells.

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Author

Summary, in English

OBJECTIVE: Periodontal ligament (PDL) cells express oestrogen receptors but the functional importance of oestrogen in PDL cells exposed to bacterial endotoxins is not known. Here we investigate if the inflammation promoter lipopolysaccharide (LPS) affects PDL cell production of interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), C-reactive protein (CRP) and/or normal functional PDL cell characteristics such as collagen synthesis and cell proliferation and if oestrogen modulates the effects of LPS. METHODS: PDL cells were obtained from periodontal ligament of premolars. PDL cells were treated with Escherichia coli LPS in the absence or presence of oestrogen (17beta-oestradiol, E(2)). Cellular concentration of IL-6, MCP-1 and CRP was determined by enzyme-linked immunosorbent assay (ELISA). Collagen synthesis was determined by l-[(3)H]proline incorporation. Cell proliferation was assessed by DNA synthesis measurement using [(3)H]thymidine incorporation. RESULTS: Stimulation with LPS (500ng/ml to 10mug/ml) increased IL-6 production in a concentration-dependent manner. Lower concentration (100ng/ml) of LPS had no effect. LPS-induced stimulation of IL-6 was not reversed by a physiologically high concentration (100nM) of E(2). LPS increased also MCP-1 production which was unaffected by E(2). Treatment with E(2) alone had no effect on either IL-6 or MCP-1. Stimulation with LPS had no effect on CRP. LPS did not affect collagen synthesis and cell proliferation, reflecting normal physiological properties of PDL cells. CONCLUSIONS: LPS stimulates PDL cell IL-6 and MCP-1 production but has no effect on the normal physiological properties of PDL cells. LPS-induced IL-6 and MCP-1 is not reversed by oestrogen suggesting that oestrogen exerts no anti-inflammatory effect via this mechanism.

Publishing year

2008

Language

English

Pages

896-902

Publication/Series

Archives of Oral Biology

Volume

Jun 11

Document type

Journal article

Publisher

Elsevier

Topic

  • Physiology

Status

Published

Research group

  • Vascular Physiology

ISBN/ISSN/Other

  • ISSN: 1879-1506