Effect of IL-6 on alveolar fibroblast proliferation in interstitial lung diseases

Clin Immunol Immunopathol. 1996 Jun;79(3):244-51. doi: 10.1006/clin.1996.0075.

Abstract

Alveolar macrophage-fibroblast interaction may be involved in the pathogenesis of interstitial lung diseases (ILD). Herein, we compared IL-6 secretion from alveolar macrophages (AM) and alveolar fibroblasts (AFb) recovered from patients with sarcoidosis (SA) and with diffuse interstitial fibrosis (DIF). Moreover, we evaluated the effect of IL-6 on the in vitro AFb proliferation in both diseases. AM and AFb from SA patients showed increased spontaneous secretion of IL-6 compared with cells from DIF subjects. Tumor necrosis factor-alpha (TNFalpha) and interleukin-1 (IL-1) enhanced IL-6 secretion and IL-6 mRNA transcription in AFb of SA patients. Addition of anti-IL-6 MoAbs increased AFb proliferation capacity in SA, but suppressed it in DIF. These results show that only SA AM and AFb secrete high levels of IL-6 which have suppressive effect on AFb proliferation. This may indicate a potential role of IL-6 in the fibrogenesis of ILD.

MeSH terms

  • Cell Division / drug effects
  • Fibroblasts / cytology
  • Gene Expression
  • Humans
  • Interleukin-1 / pharmacology
  • Interleukin-6 / physiology*
  • Lung Diseases, Interstitial / metabolism
  • Lung Diseases, Interstitial / pathology*
  • Macrophages, Alveolar / physiology
  • Pulmonary Alveoli / cytology*
  • RNA, Messenger / metabolism
  • Sarcoidosis / metabolism
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

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