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Articles in PresS, published online ahead of print October 4, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00168.2002
Submitted on May 30, 2002
Accepted on September 27, 2002
1 Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA
2 College of Natural Sciences, University of Texas, Austin, TX, USA
* To whom correspondence should be addressed. E-mail: BMoore{at}umich.edu.
CCR2 -/- mice are protected from experimental pulmonary fibrosis, a disease increasingly recognized as being mediated by dysfunctional interactions between epithelial cells and fibroblasts. We have sought to investigate the interactions between alveolar epithelial cells (AECs) and fibroblasts in these fibrosis-resistant (CCR2 -/-) and fibrosis-sensitive (CCR2 +/+) mice. AECs from CCR2 -/- mice suppress fibroblast proliferation more than AECs from CCR2 +/+ mice (77% vs. 43%). Exogenous administration of the CCR2 ligand MCP-1 to the fibroblast-AEC co-cultures reverses the suppression mediated by CCR2 +/+ AECs, but has no effect with CCR2 -/- AECs. MCP-1 regulates AEC function, but not fibroblast function. AEC inhibition of fibroblast proliferation was mediated by a soluble, aspirin-sensitive factor. Accordingly, AECs from CCR2 -/- mice produce greater quantities of PGE2, than do AECs from CCR2 +/+ mice and MCP-1 inhibits AEC-derived PGE2 synthesis. Diminished PGE2 production by AECs results in enhanced fibroproliferation. Thus, an important pro-fibrotic mechanism of MCP-1/CCR2 interactions is to limit PGE2 production in AECs following injury, thus promoting fibrogenesis.
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