Effects of TNF-α and IL-1 β on the activation of genes related to inflammatory, immune responses and cell death in immortalized human HaCat keratinocytes

Int J Immunopathol Pharmacol. 2010 Oct-Dec;23(4):1057-72. doi: 10.1177/039463201002300410.

Abstract

The present experiments were designed to characterize by microarray analysis the transcriptional responses of human keratinocytes (HaCat) to TNF-α and IL-1 β, given alone or in combination, in order to better understand the mechanisms underlying inflammatory, immune responses and cell death in which both cytokines play a pathophysiological role. Significant differences in the percentage and quality of genes dysregulated by TNF-α and IL-1 β were shown. Both cytokines activated a series of genes involved in inflammatory, immune response as well as in cell death. In our experimental conditions, TNF-α, in contrast to IL-1 β, did not induce a significant level of apoptosis in keratinocytes. However, given together both cytokines produced a significant decrease in apoptotic cells and synergistic transcriptional response which was due to the activation of several specific genes occurring after application of each cytokine. TNF-α and IL-1 β evoked apoptotic effect and transcriptional responses were linked to the stimulation of their specific receptors since a pre-treatment with monoclonal antibodies vs TNF-α and/or IL-1 β receptors was able to significantly reduce them.

MeSH terms

  • Apoptosis / drug effects*
  • Cell Survival / drug effects
  • Cells, Cultured
  • Chemokines / biosynthesis
  • Gene Expression Profiling*
  • Humans
  • Interleukin-1beta / pharmacology*
  • Keratinocytes / drug effects*
  • Keratinocytes / immunology
  • Keratinocytes / metabolism
  • Oligonucleotide Array Sequence Analysis
  • Transcriptional Activation / drug effects*
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Chemokines
  • Interleukin-1beta
  • Tumor Necrosis Factor-alpha