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Induction and Characterization of Pulmonary Hypertension in Mice using the Hypoxia/SU5416 Model
Published on: June 3, 2020
SP-D-deficient mice are resistant to hyperoxia
Deepika Jain1, Elena Atochina-Vasserman, Helchem Kadire
1Pulmonary and Critical Care Division, University of Pennsylvania School of Medicine, Room H410F, Hill Pavilion, 380 South University Ave., Philadelphia, PA 19107, USA.
American Journal of Physiology. Lung Cellular and Molecular Physiology
|December 13, 2006
Summary
Mice lacking surfactant protein D (SP-D) showed increased survival during hyperoxia, suggesting SP-D deficiency confers resistance to lung injury through surfactant changes and altered immune responses.
Area of Science:
- Pulmonary immunology
- Innate immunity
- Respiratory physiology
Background:
- Surfactant protein D (SP-D) is a collectin involved in lung inflammation and immunity.
- SP-D gene disruption in mice leads to lung inflammation and emphysema.
- The role of SP-D in hyperoxia-induced lung injury is not well understood.
Purpose of the Study:
- To investigate the effect of SP-D deficiency on hyperoxia-induced lung injury.
- To determine if SP-D absence influences survival and lung pathology during hyperoxia.
Main Methods:
- SP-D-deficient (SP-D-/-) and wild-type (SP-D+/+) mice were exposed to 80% oxygen for 14 days.
- Survival rates, histopathological injury scores, bronchoalveolar lavage (BAL) fluid analysis, and lung biochemistry were assessed.
- Surfactant biophysical activity and BAL cytokine profiles were analyzed.
Main Results:
- SP-D-/- mice exhibited 100% survival during hyperoxia, contrasting with 30% survival in SP-D+/+ mice.
- SP-D-/- mice showed reduced histopathological injury scores despite increased BAL cells and neutrophils.
- Biochemical analysis revealed higher surfactant phospholipid and SP-B levels in SP-D-/- mice, preserving surfactant activity.
Conclusions:
- SP-D deficiency confers resistance to hyperoxia-induced lung injury.
- This resistance is associated with enhanced surfactant function and altered pulmonary immune cell profiles.
- Homeostatic adaptations in SP-D-/- mice, including surfactant changes and cytokine modulation, contribute to lung protection.
