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Injecting LPS into the amniotic fluid of Tie2- lacZ endothelial reporter mice at embryonic day 15 stimulated angiogenesis in the saccular stage fetal lung mesenchyme. LPS also increased the number of endothelial cells in saccular stage fetal mouse lung explants. Inflammation appeared to directly promote vascular development, as LPS stimulated pulmonary microvascular endothelial cell angiogenesis, cell migration, and proliferation in vitro. Whereas LPS did not increase expression of VEGF, angiopoietin-1 (Ang-1), Tie2, fetal liver kinase-1 (Flk-1), fms-like tyrosine kinase-1 (Flt-1), PDGFA, PDGFB, heparin-binding EGF-like growth factor (HB-EGF), or connective tissue growth factor (CTGF), LPS did stimulate the production of the angiogenic CC chemokines macrophage inflammatory protein-1\u03b1 (MIP-1\u03b1) and monocyte chemoattractant protein-1 (MCP-1). Both MIP-1\u03b1 and MCP-1 increased angiogenesis in fetal mouse lung explants. In addition, inhibitory antibodies against MIP-1\u03b1 and MCP-1 blocked the effects of LPS on fetal lung vascular development, suggesting these chemokines are downstream mediators of LPS-induced angiogenesis. We speculate that an inflammation-mediated surge in angiogenesis could lead to formation of aberrant alveolar capillaries in the lungs of patients developing BPD.<\/jats:p>","DOI":"10.1152\/ajplung.00414.2009","type":"journal-article","created":{"date-parts":[[2010,2,20]],"date-time":"2010-02-20T02:00:25Z","timestamp":1266631225000},"page":"L637-L645","source":"Crossref","is-referenced-by-count":53,"title":["Chorioamnionitis stimulates angiogenesis in saccular stage fetal lungs via CC chemokines"],"prefix":"10.1152","volume":"298","author":[{"given":"J. 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