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Am J Physiol Lung Cell Mol Physiol (May 3, 2002). doi:10.1152/ajplung.00048.2002
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Articles in PresS, published online ahead of print May 3, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00048.2002
Submitted on February 1, 2002
Accepted on April 25, 2002

Angiogenic growth factors in the pathophysiology of a murine model of acute lung injury

Dimitrios Karmpaliotis1, Ioanna Kosmidou1, Edward P. Ingenito1, Kailin Hong1, Atul Malhotra1, Mary E. Sunday1, and Kathleen J. Haley1*

1 Division of Pulmonary and Critical Care Medicine and Department of Pathology, Brigham and Women's Hosptial, Boston, MA, USA

* To whom correspondence should be addressed. E-mail: khaley{at}rics.bwh.harvard.edu.

Capillary leakage and alveolar edema are hallmarks of Acute Lung Injury (ALI). Neutrophils and serum macromolecules enter alveoli, promoting inflammation. Vascular endothelial growth factor (VEGF) causes plasma leakage in extra-pulmonary vessels. Angiopoietin-1 (Ang-1) and 4 (Ang-4) stabilize vessels, attenuating capillary leakage. We hypothesized that VEGF and Ang-1/4 modulate vessel leakage in the lung, contributing to the pathogenesis of ALI. We examined a murine model of lipopolysacharide (LPS)-induced ALI. C57BL/6 and 129/J mice were studied at baseline and 24, 48, and 96 hours after single or multiple doses of aerosolized LPS. Both strains exhibited time and dose-dependent increases in inflammation, and a deterioration of lung mechanics. BAL protein levels increased significantly suggesting capillary leakage. Increased BAL neutrophil and total protein content correlated with time-dependent increased tissue VEGF and decreased Ang-1/4 levels, with peak VEGF and minimum Ang-1/4 expression after 96 hours of LPS challenge. These data suggest that changes in the balance between VEGF and Ang-1/4 after LPS exposure may modulate neutrophil influx, protein leakage and alveolar flooding during early ALI.




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