PMID- 18554572 OWN - NLM STAT- MEDLINE DCOM- 20090209 LR - 20080722 IS - 0003-9969 (Print) IS - 0003-9969 (Linking) VI - 53 IP - 9 DP - 2008 Sep TI - LPS-induced MCP-1 and IL-6 production is not reversed by oestrogen in human periodontal ligament cells. PG - 896-902 LID - 10.1016/j.archoralbio.2008.05.001 [doi] AB - 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, E2). Cellular concentration of IL-6, MCP-1 and CRP was determined by enzyme-linked immunosorbent assay (ELISA). Collagen synthesis was determined by l-[3H]proline incorporation. Cell proliferation was assessed by DNA synthesis measurement using [3H]thymidine incorporation. RESULTS: Stimulation with LPS (500 ng/ml to 10 microg/ml) increased IL-6 production in a concentration-dependent manner. Lower concentration (100 ng/ml) of LPS had no effect. LPS-induced stimulation of IL-6 was not reversed by a physiologically high concentration (100 nM) of E2. LPS increased also MCP-1 production which was unaffected by E2. Treatment with E2 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. FAU - Jonsson, Daniel AU - Jonsson D AD - Department of Periodontology, Faculty of Odontology, Malmo University, SE-205 06 Malmo, Sweden. daniel.jonsson@od.mah.se FAU - Nebel, Daniel AU - Nebel D FAU - Bratthall, Gunilla AU - Bratthall G FAU - Nilsson, Bengt-Olof AU - Nilsson BO LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20080612 PL - England TA - Arch Oral Biol JT - Archives of oral biology JID - 0116711 RN - 0 (Chemokine CCL2) RN - 0 (Estrogens) RN - 0 (Interleukin-6) RN - 0 (Lipopolysaccharides) RN - 0 (Receptors, Estrogen) RN - 9007-41-4 (C-Reactive Protein) SB - IM MH - Adolescent MH - C-Reactive Protein/metabolism MH - Cells, Cultured/metabolism MH - Chemokine CCL2/*metabolism/pharmacology MH - Child MH - Estrogens/*pharmacology MH - Female MH - Humans MH - Interleukin-6/metabolism MH - Lipopolysaccharides/pharmacology MH - Periodontal Ligament/drug effects/*metabolism MH - Receptors, Estrogen/*metabolism EDAT- 2008/06/17 09:00 MHDA- 2009/02/10 09:00 CRDT- 2008/06/17 09:00 PHST- 2007/10/24 00:00 [received] PHST- 2008/03/25 00:00 [revised] PHST- 2008/05/01 00:00 [accepted] PHST- 2008/06/17 09:00 [pubmed] PHST- 2009/02/10 09:00 [medline] PHST- 2008/06/17 09:00 [entrez] AID - S0003-9969(08)00139-8 [pii] AID - 10.1016/j.archoralbio.2008.05.001 [doi] PST - ppublish SO - Arch Oral Biol. 2008 Sep;53(9):896-902. doi: 10.1016/j.archoralbio.2008.05.001. Epub 2008 Jun 12.