Effect of lipopolysaccharide and transforming growth factor-beta 1 on expression and signal pathway of Toll like receptor 4 in dental pulp cells.
- Author:
Wenhua DU
1
;
Minhua JIA
Author Information
- Publication Type:Journal Article
- MeSH: Dental Pulp; Epithelial Cells; Humans; Interleukin-6; Lipopolysaccharides; NF-kappa B; Signal Transduction; Toll-Like Receptor 4; Transforming Growth Factor beta; Transforming Growth Factor beta1
- From: West China Journal of Stomatology 2012;30(1):77-86
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the expression of Toll like receptor 4 (TLR4) on the pulp cells and the change of related signaling molecules under the condition of concomitant lipopolysaccharide (LPS) and transforming growth factor-beta 1 (TGF-beta 1) during the course of pulpitis.
METHODSAfter treated by LPS and TGF-beta 1, the expression of TLR4 on pulp cells was detected by flow cytometry (FCM). The expressions of signaling molecules evolutionarily conserved signaling intermediate in Toll pathways (ECSIT) and nuclear factor-kappaB (NF-kappaB) were detected by real-time polymerase chain reaction (real-time PCR) and Western blot. The secretion of interleukin-6 (IL-6) was detected by enzyme-linked immunosorbent assay (ELISA). Furthermore, the change of corresponding targets in inflamed pulp cells from clinical samples were detected by real-time PCR.
RESULTSAfter treated by LPS and TGF-beta 1 in vitro, there was no change in the expression of TLR4 on pulp cells, but the secretion of proinflammatory cytokines IL-6 increased. LPS and TGF-beta 1 could also increase the expression of signal downstream ECSIT and actived NF-kappaB. Furthermore, the expression of TLR4 mRNA had no increase in inflamed pulp cells from clinical samples, while the expression of TGF-beta 1, ECSIT and IL-6 mRNA increased through real-time PCR.
CONCLUSIONDuring the course of pulpitis, although the expression of TLR4 on pulp cells was inhibited by increased expression of TGF-beta 1, the TLR4 pathway was still activated. This effect could be caused through activation of ECSIT mediated by LPS, which might inhibit the TGF-beta 1 pathway.