LPS induces IL-8 expression through TLR4, MyD88, NF-kappaB and MAPK pathways in human dental pulp stem cells

Int Endod J. 2013 Feb;46(2):128-36. doi: 10.1111/j.1365-2591.2012.02096.x. Epub 2012 Jul 12.

Abstract

Aim: To evaluate the effects of lipopolysaccharide (LPS) on interleukin-8 (IL-8) and related intracellular signalling pathways in human dental pulp stem cells (hDPSCs).

Methodology: Human pulp tissues were isolated from human impacted third molars, and the hDPSCs were cultured and characterized. The effects of LPS on IL-8 and Toll-like receptor 4 (TLR4) gene expression in hDPSCs were investigated using real-time quantitative RT-PCR and ELISA. Whether TLR4/MyD88/NF-кB was involved in the LPS-induced up-regulation of IL-8 in hDPSCs was determined using transient transfection, luciferase assay and ELISA. The involvement of MAPKs in the LPS-induced up-regulation of IL-8 in hDPSCs was investigated via transient transfection, luciferase assay, ELISA and western blot. The data were statistically analysed using Student's t-test or one-way anova followed by the Student-Neumann-Keuls test.

Results: Cells exposed to LPS not only displayed an enhanced expression of TLR4 but also showed an elevated IL-8 gene expression; exposure to LPS also resulted in the induction of IL-8 gene transcription via promoter activation. The LPS-induced IL-8 promoter activation was inhibited through dominant-negative mutations in TLR4 and MyD88, but not in TLR2. The LPS-induced IL-8 protein release was attenuated through the administration of TLR4-neutralizing antibody or MyD88 inhibitory peptide and a dominant-negative mutation in IκBα. In contrast, IL-8 protein release was enhanced through the expression of NF-κB p65. Treatment with PDTC, TPCK or Bay117082 effectively antagonized LPS-induced IL-8 protein release. Moreover, both the promoter activity and the LPS-induced release of IL-8 were diminished upon the administration of U0126 and SB203580, but not SP600125. Moreover, the exposure to LPS activated ERK1/2 and p38 MAPK phosphorylation in cells.

Conclusions: This study reports the LPS-mediated transcriptional and post-translational up-regulation of IL-8, which is a process that also involves TLR4, MyD88, NF-κB and MAPK.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Analysis of Variance
  • Cells, Cultured
  • Dental Pulp / cytology
  • Dental Pulp / drug effects
  • Dental Pulp / metabolism*
  • Gene Expression Regulation*
  • Humans
  • Immunophenotyping
  • Interleukin-8 / biosynthesis*
  • Interleukin-8 / genetics
  • Lipopolysaccharides / pharmacology
  • MAP Kinase Signaling System
  • Myeloid Differentiation Factor 88 / genetics
  • Myeloid Differentiation Factor 88 / metabolism
  • NF-kappa B / genetics
  • NF-kappa B / metabolism
  • Promoter Regions, Genetic
  • Real-Time Polymerase Chain Reaction
  • Signal Transduction*
  • Stem Cells / drug effects
  • Stem Cells / metabolism*
  • Toll-Like Receptor 4 / biosynthesis*
  • Toll-Like Receptor 4 / genetics
  • Transfection
  • Up-Regulation
  • Young Adult

Substances

  • Interleukin-8
  • Lipopolysaccharides
  • Myeloid Differentiation Factor 88
  • NF-kappa B
  • Toll-Like Receptor 4