Priming of alveolar macrophages for interleukin-8 production in patients with idiopathic pulmonary fibrosis

Am J Respir Crit Care Med. 1995 Nov;152(5 Pt 1):1579-86. doi: 10.1164/ajrccm.152.5.7582298.


We evaluated the contribution of interleukin-8 (IL-8) to the pathogenesis of idiopathic pulmonary fibrosis (IPF) by studying bronchoalveolar lavage fluid (BALF) in eight patients with IPF in the chronically progressive phase, five patients with IPF in the subacutely progressive phase, eight patients with sarcoidosis (SAR), and eight control (CTL) subjects. IL-8 levels were not increased in the BALF of the patients with IPF in the chronic phase (11.3 +/- 8.8 pg/ml), nor in that of the SAR patients (13.8 +/- 7.8 pg/ml), whereas they were increased in the BALF of patients with IPF in the subacutely progressive phase (1.93 +/- 1.10 ng/ml). We then investigated extracellular and cell-associated IL-8 in lipopolysaccharide (LPS)-stimulated BALF cells to determine the IL-8-producing potential of alveolar macrophages (AM). Following LPS stimulation of BALF cells from patients with IPF in the chronic phase, both the extracellular IL-8 in culture fluid and the cell-associated IL-8 in AM were increased as compared with those for the CTL subjects (p < 0.05 and p < 0.05, respectively). These results suggest that AM of patients with IPF are primed for IL-8 production. We conclude that IL-8 may play a role in neutrophilic alveolitis, especially during the subacute phase of IPF.

Publication types

  • Comparative Study

MeSH terms

  • Acute Disease
  • Adult
  • Aged
  • Aged, 80 and over
  • Analysis of Variance
  • Bronchoalveolar Lavage Fluid / chemistry
  • Bronchoalveolar Lavage Fluid / cytology
  • Chemotaxis, Leukocyte
  • Chronic Disease
  • Escherichia coli
  • Female
  • Humans
  • Interleukin-8 / analysis
  • Interleukin-8 / biosynthesis*
  • Lipopolysaccharides / pharmacology
  • Macrophage Activation* / drug effects
  • Macrophages, Alveolar / drug effects
  • Macrophages, Alveolar / metabolism*
  • Male
  • Middle Aged
  • Neutrophils / physiology
  • Pulmonary Fibrosis / etiology
  • Pulmonary Fibrosis / metabolism*
  • Pulmonary Fibrosis / pathology
  • Sarcoidosis, Pulmonary / metabolism
  • Sarcoidosis, Pulmonary / pathology
  • Stimulation, Chemical


  • Interleukin-8
  • Lipopolysaccharides