Expression of monocyte chemoattractant protein 1 mRNA in human idiopathic pulmonary fibrosis

Proc Natl Acad Sci U S A. 1992 Jun 15;89(12):5371-5. doi: 10.1073/pnas.89.12.5371.

Abstract

Macrophages are thought to play an important role in the pathologic changes associated with idiopathic pulmonary fibrosis (IPF). The mechanisms for increased monocyte/macrophage recruitment in IPF are unknown. Monocyte chemoattractant protein 1 (MCP-1) is the predominant monocyte chemoattractant secreted by a variety of different cell types in culture. We examined the expression of MCP-1 mRNA and its protein product in vivo in IPF and non-IPF lung specimens by in situ hybridization and immunocytochemistry. The cell types expressing MCP-1 in vivo were identified by immunostaining with specific antibodies. We demonstrated the expression of MCP-1 mRNA in pulmonary epithelial cells, in monocytes/macrophages, and in vascular endothelial and smooth muscle cells. Lung epithelial cells in patients with IPF strongly expressed MCP-1 mRNA and its protein product. In contrast, epithelial cells in non-IPF specimens did not express MCP-1 mRNA. Macrophages and vascular endothelial and smooth muscle cells were shown to express MCP-1 in both IPF and non-IPF lung specimens. These findings provide a basis for the understanding of the in vivo physiologic processes that mediate monocyte/macrophage recruitment and infiltration in the lung interstitium and the pathologic state contributing to an increased alveolar monocyte/macrophage population and inflammation in IPF.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Arteries / metabolism
  • Arteries / pathology
  • Biopsy
  • Chemokine CCL2
  • Chemotactic Factors / genetics*
  • Endothelium, Vascular / metabolism
  • Endothelium, Vascular / pathology
  • Epithelium / metabolism
  • Epithelium / pathology
  • Humans
  • Lung / metabolism
  • Lung / pathology
  • Muscle, Smooth, Vascular / metabolism
  • Muscle, Smooth, Vascular / pathology
  • Nucleic Acid Hybridization
  • Pulmonary Circulation
  • Pulmonary Fibrosis / genetics*
  • Pulmonary Fibrosis / metabolism
  • Pulmonary Fibrosis / pathology
  • RNA Probes
  • RNA, Messenger / analysis
  • RNA, Messenger / genetics*
  • RNA, Messenger / metabolism

Substances

  • Chemokine CCL2
  • Chemotactic Factors
  • RNA Probes
  • RNA, Messenger