Expression of monocyte chemoattractant protein 1 mRNA in human idiopathic pulmonary fibrosis.
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.
Antoniades
H N
HN
Center for Blood Research, Harvard School of Public Health, Boston, MA 02115.
Neville-Golden
J
J
Galanopoulos
T
T
Kradin
R L
RL
Valente
A J
AJ
Graves
D T
DT
D001158:Arteries / Q000378:metabolism / Q000473:pathology; D001706:Biopsy; D018932:Chemokine CCL2; D002630:Chemotactic Factors / Q000235:genetics*; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology; D004848:Epithelium / Q000378:metabolism / Q000473:pathology; D006801:Humans; D008168:Lung / Q000378:metabolism / Q000473:pathology; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology; D009693:Nucleic Acid Hybridization; D011652:Pulmonary Circulation; D011658:Pulmonary Fibrosis / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D015347:RNA Probes; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics* / Q000378:metabolism
D018932:Chemokine CCL2; D002630:Chemotactic Factors; D015347:RNA Probes; D012333:RNA, Messenger