Tumor necrosis factor-induced interleukin-8 expression in cultured human airway epithelial cells

Am J Physiol. 1994 Oct;267(4 Pt 1):L398-405. doi: 10.1152/ajplung.1994.267.4.L398.

Abstract

The effects of tumor necrosis factor-alpha (TNF-alpha) on interleukin-8 (IL-8) expression and generation were examined in primary cultured human airway epithelial cells (HAEC) and a human lung epithelial cell line (A549). TNF-alpha increased IL-8 mRNA and protein expression in HAEC in a concentration- and time-dependent manner and these effects were inhibited by dexamethasone (1 microM). There was no change in the stability of IL-8 mRNA, and a nuclear run-on assay confirmed that TNF-alpha increased IL-8 gene transcription. TNF-alpha-induced IL-8 mRNA expression showed a biphasic response in HAEC, with an early increase at 2 h followed by a sustained increase from 8 h, which was abolished by the addition of cycloheximide, suggesting that the synthesis of another protein was involved. A549 cells also increased IL-8 secretion and mRNA after incubation of TNF-alpha, with inhibition by dexamethasone. However, A549 cells showed only an early single peak. A549 cells showed a 250-fold increase in the generation of IL-8 immunoreactivity, whereas primary cultured HAEC showed only a threefold increase, suggesting that HAEC and A549 cells may respond to TNF-alpha in different ways. The sustained increase in IL-8 secretion due to an increase in gene transcription in response to TNF-alpha may be an important amplification step in inflammatory diseases of the airways.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bronchi / cytology
  • Bronchi / metabolism*
  • Cell Line
  • Cells, Cultured
  • Cycloheximide / pharmacology
  • Dexamethasone / pharmacology
  • Epithelial Cells
  • Epithelium / metabolism
  • Half-Life
  • Humans
  • Interleukin-8 / genetics
  • Interleukin-8 / metabolism*
  • Lung / cytology
  • Lung / metabolism*
  • RNA, Messenger / metabolism
  • Trachea / cytology
  • Trachea / metabolism*
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Interleukin-8
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Dexamethasone
  • Cycloheximide