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produces an increase
in lung volumes and pulmonary hypertension
1 Department of Medicine, National Jewish Medical and Research Center, Denver 80206; and 2 Cardiovascular Pulmonary Research Laboratory, University of Colorado Health Science Center, Denver, Colorado 80262
Tumor necrosis factor
(TNF)-
is a key proinflammatory cytokine that is thought to be
important in the development of pulmonary fibrosis, whereas its role in
pulmonary emphysema has not been as thoroughly documented. In the
present study, TNF- was overexpressed in alveolar type II cells
under the control of the human surfactant protein C promoter. In this
report, we further characterized the pulmonary abnormalities and
provided a physiological assessment of these mice. Histopathology of
the lungs revealed chronic inflammation, severe alveolar air space
enlargement and septal destruction, and bronchiolitis. However,
pulmonary fibrosis was very limited and only seen in the subpleural,
peribronchiolar, and perivascular regions. Physiological assessment
showed an increase in lung volumes and a decrease in elastic recoil
characteristic of emphysema; there was no evidence of restrictive lung
disease characteristic of pulmonary fibrosis. In addition, the mice
raised in ambient conditions in Denver developed pulmonary
hypertension. Gelatinase activity was increased in the lavage fluid
from these lungs. These results suggest that in these mice TNF-
contributed to the development of pulmonary emphysema through chronic
lung inflammation and activation of the elastolytic enzymes but by
itself was unable to produce significant pulmonary fibrosis.
emphysema; pulmonary fibrosis; pulmonary hypertension
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