Phenotypic features of alveolar monocytes/macrophages and IL-8 gene activation by IL-1 and TNF-alpha in asthmatic patients

Allergy. 2000;55 Suppl 61:36-41. doi: 10.1034/j.1398-9995.2000.00505.x.


The alveolar macrophage (AM), a major defense cell in the lung, participates in immune and inflammatory reactions through the release of several regulatory and chemotactic cytokines. In particular, macrophages are considered to play a pivotal proinflammatory role in the production and maintenance of airway inflammation and bronchial hyperreactivity. To assess the phenotypic pattern of AM from asthmatic subjects, we performed the following experiments: 1) cytofluorometric analysis of specific phenotypic features (CD11b, CD14, CD16, CD45, HLA-DR, CD71, CD95, and CD44) 2) assessment of the production of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1, and the chemotactic regulatory cytokine IL-8 by unstimulated and lipopolysaccharide-stimulated AM. In these patients, we phenotypically characterized the AM, showing their strong proinflammatory activity also in patients with mild asthma. Their activity has been clarified by our biomolecular data that showed a constitutive basal IL-8 production by AM, and also indicated that IL-1 and TNF-alpha were able to upregulate the ability of activated human AM to produce IL-8 at the protein and messenger ribonucleic acid (mRNA) levels.

MeSH terms

  • Asthma / immunology
  • Asthma / physiopathology*
  • Cytokines / genetics
  • Cytokines / metabolism
  • Gene Expression Regulation
  • Humans
  • Interleukin-1 / metabolism*
  • Interleukin-1 / pharmacology
  • Interleukin-8 / biosynthesis
  • Interleukin-8 / genetics*
  • Lipopolysaccharides / pharmacology
  • Macrophage Activation
  • Macrophages, Alveolar / immunology*
  • Macrophages, Alveolar / metabolism
  • Monocytes / immunology
  • Monocytes / metabolism
  • Phenotype
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Transcription, Genetic
  • Transcriptional Activation
  • Tumor Necrosis Factor-alpha / metabolism*
  • Tumor Necrosis Factor-alpha / pharmacology


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