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Am J Physiol Lung Cell Mol Physiol 280: L1148-L1156, 2001;
1040-0605/01 $5.00
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Vol. 280, Issue 6, L1148-L1156, June 2001

GM-CSF mediates alveolar macrophage proliferation and type II cell hypertrophy in SP-D gene-targeted mice

Samuel Hawgood, Jennifer Akiyama, Cynthia Brown, Lennell Allen, Gordon Li, and Francis R. Poulain

Department of Pediatrics, Cardiovascular Research Institute, University of California, San Francisco, California 94118-1245

Mice deficient in surfactant protein (SP) D develop increased surfactant pool sizes and dramatic changes in alveolar macrophages and type II cells. To test the hypothesis that granulocyte-macrophage colony-stimulating factor (GM-CSF) mediates alveolar macrophage proliferation and activation and the type II cell hypertrophy seen in SP-D null mice, we bred SP-D and GM-CSF gene-targeted mice to obtain littermate double null, single null, and wild-type mice. Bronchoalveolar lavage levels of phospholipid, protein, SP-D, SP-A, and GM-CSF were measured from 1 to 4 mo. There was an approximately additive accumulation of phospholipid, total protein, and SP-A at each time point. Microscopy showed normal macrophage number and morphology in GM-CSF null mice, numerous giant foamy macrophages and hypertrophic type II cells in SP-D null mice, and large but not foamy macrophages and mostly normal type II cells in double null mice. These results suggest that the mechanisms underlying the alveolar surfactant accumulation in the SP-D-deficient and GM-CSF-deficient mice are different and that GM-CSF mediates some of the macrophage and type II cell changes seen in SP-D null mice.

lung surfactant; granulocyte-macrophage colony-stimulating factor; type II cells; inflammation; surfactant protein D


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