Expression of IL-8 gene in human monocytes and lymphocytes: differential regulation by TNF and IL-1

Cytokine. 2000 Jun;12(6):636-43. doi: 10.1006/cyto.1999.0664.

Abstract

TNF-alpha and IL-1 were reported to be the most powerful inducers of IL-8 in a multitude of cells, including leukocytes. In this study, we investigated TNF-alpha- and IL-1-mediated regulation of IL-8 gene expression in non-fractionated PBMC, and purified monocyte (MO) and lymphocyte (LY) fractions. Our analysis revealed that purified human MO did not respond to exogenous TNF-alpha with the induction of IL-8 mRNA or protein, nor require endogenous TNF-alpha for IL-8 expression. In contrast, in the presence of exogenous IL-1alpha and IL-1beta a substantial enhancement of IL-8 mRNA and protein expression in MO was observed. Nevertheless, antibodies to IL-1alpha and IL-1beta were unable to downregulate the expression of IL-8 in resting adherent or Staphylococcus aureus Cowan 1 (SAC)-stimulated MO. In contrast with MO, purified LY and non-fractionated PBMC expressed IL-8 in response to exogenous TNF-alpha, similar to exogenous IL-1alpha and IL-1beta. As was seen with MO, antibodies to TNF-alpha, IL-1alpha and IL-1beta did not inhibit the expression of IL-8 in purified LY and non-fractionated PBMC stimulated with SAC and LPS. Taken together, our data demonstrate major differences in responsiveness of MO and LY to exogenous TNF-alpha and IL-1, and suggest relative autonomy of IL-8 gene expression in these cells that does not require accessory cytokines but can be induced directly by exogenous stimuli.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Adhesion
  • Gene Expression Regulation / drug effects
  • Gene Expression Regulation / immunology*
  • Humans
  • In Vitro Techniques
  • Interleukin-1 / pharmacology*
  • Lymphocytes / drug effects
  • Lymphocytes / immunology*
  • Monocytes / drug effects
  • Monocytes / immunology*
  • Protein Biosynthesis / drug effects
  • Protein Biosynthesis / immunology
  • RNA, Messenger / genetics
  • Staphylococcus aureus / immunology
  • Transcription, Genetic / drug effects
  • Transcription, Genetic / immunology
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Interleukin-1
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha