Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1992-7-21
pubmed:abstractText
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.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-1695010, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-1846446, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-2113354, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-2121752, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-2170444, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-2313097, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-2406243, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-2435682, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-2465924, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-2513477, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-2781291, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-2787988, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-2919636, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-3415979, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-3522217, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-3543052, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-3600711, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-6183346, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-6191602, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-6630527, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-6839345, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-6872001, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-7140934, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-7227337, http://linkedlifedata.com/resource/pubmed/commentcorrection/1608944-7382428
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0027-8424
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
89
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5371-5
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Expression of monocyte chemoattractant protein 1 mRNA in human idiopathic pulmonary fibrosis.
pubmed:affiliation
Center for Blood Research, Harvard School of Public Health, Boston, MA 02115.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't