Increased production of interleukin 6 and interleukin 8 in scleroderma fibroblasts

J Rheumatol. 1998 Feb;25(2):296-301.

Abstract

Objective: To determine additional abnormal characteristics related to cytokines in fibroblasts derived from systemic sclerosis (SSc), we examined the production of interleukin 6 (IL-6) and IL-8 and their mRNA levels both in scleroderma fibroblasts and in those from normal skin.

Methods: Cultured fibroblasts from patients with SSc and healthy controls were examined. Production of IL-6 and IL-8 was assessed by specific ELISA, and the levels of IL-6 and IL-8 mRNA were determined by reverse transcriptase polymerase chain reaction (RT-PCR).

Results: Basal production of both IL-6 and IL-8 was significantly increased in scleroderma fibroblasts compared with controls. When cells were stimulated with either IL-1beta (50 pg/ml) or tumor necrosis factor-alpha (TNF-alpha: 10 ng/ml), the production of IL-6 and IL-8 was predominantly increased in both cell strains and there was no significant difference in the production of IL-6 and IL-8 between them. When normal fibroblasts were stimulated with IL-1beta for 48 h and subcultured, both IL-6 and IL-8 production were significantly increased, and production remained elevated even after 3 passages. RT-PCR revealed that IL-6 and IL-8 mRNA were detected in scleroderma fibroblasts but not in normal skin fibroblasts without cytokine stimulation. When stimulated with IL-1beta, both cell strains expressed IL-6 and IL-8 mRNA to almost the same extent.

Conclusion: Increased production of IL-6 and IL-8 by scleroderma fibroblasts suggests that these cells may have been stimulated by certain cytokines in vivo.

MeSH terms

  • Cells, Cultured
  • Fibroblasts / drug effects
  • Fibroblasts / metabolism
  • Humans
  • Interleukin-1 / pharmacology
  • Interleukin-6 / blood
  • Interleukin-6 / metabolism*
  • Interleukin-8 / blood
  • Interleukin-8 / metabolism*
  • Polymerase Chain Reaction
  • RNA, Messenger / analysis
  • Scleroderma, Systemic / metabolism*
  • Transcription, Genetic
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Interleukin-1
  • Interleukin-6
  • Interleukin-8
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha