Evaluation of alveolar macrophages in normals and individuals with active pulmonary sarcoidosis for the spontaneous expression of the interleukin-1 beta gene. Academic Article uri icon

Overview

MeSH

  • Gene Expression Regulation
  • Humans
  • Immunosorbent Techniques
  • Lung
  • Pulmonary Alveoli
  • RNA, Messenger

MeSH Major

  • Interleukin-1
  • Lung Diseases
  • Macrophages
  • Sarcoidosis

abstract

  • We have evaluated the hypothesis that the presence of large numbers of activated helper/inducer T lymphocytes in the lungs of individuals with active pulmonary sarcoidosis is associated with the exaggerated release of interleukin-1 (IL-1) by alveolar macrophages. Evaluation of media from unstimulated cultured sarcoid alveolar macrophages failed to detect IL-1 activity. When parallel cultures of sarcoid and normal alveolar macrophages were stimulated with lipopolysaccharide (LPS), they released similar amounts of IL-1 activity. Using a highly specific polyclonal anti-IL-1 beta antibody and flow cytometry to evaluate cell-associated IL-1 beta, analysis of fresh alveolar macrophages from patients with active sarcoidosis and normal individuals revealed no detectable cell-associated IL-1 beta, but IL-1 beta was present when macrophages from sarcoid patients and normals were stimulated with LPS. Similar observations were made using immunoblot analysis of cell lysates of the same unstimulated and stimulated macrophages. Finally, Northern analysis of alveolar macrophages for IL-1 beta mRNA transcripts demonstrated minimal, but equivalent, amounts of IL-1 beta in both normal and sarcoid macrophages, as compared to the much larger quantities present in LPS-stimulated alveolar macrophages. Thus, while alveolar macrophages of individuals with sarcoidosis are clearly capable of expressing the IL-1 beta gene, these findings suggest that altered expression of the IL-1 beta gene by alveolar macrophages does not play a central role in the exaggerated lung T-cell activation characteristic of sarcoidosis.

publication date

  • July 1987

has subject area

  • Gene Expression Regulation
  • Humans
  • Immunosorbent Techniques
  • Interleukin-1
  • Lung
  • Lung Diseases
  • Macrophages
  • Pulmonary Alveoli
  • RNA, Messenger
  • Sarcoidosis

Research

keywords

  • Journal Article

Identity

Language

  • eng

PubMed ID

  • 3297354

Additional Document Info

start page

  • 479

end page

  • 488

volume

  • 107

number

  • 2