Surfactant protein-B (SP-B) is a small, hydrophobic pcptide that plays a critical role in pulmonary function and surfactant homeostasis. To determine whether SP-B protects mice from oxygen-induced injury, heterozygous SP-B+/- gene-targeted mice and wild-type SP-B+/+ littermates were exposed to hyperoxia (95% oxygen for 3 d) or room air. Although specific lung compliance in room air in SP-B+/- mice was slightly reduced as compared with that in SP-B+/+ mice, it was reduced more markedly during hyperoxia (46% versus 25% decrease, respectively). The larger decrease in lung compliance in SP-B+/- mice was associated with increased severity of pulmonary edema, hemorrhage and inflammation, lung permeability and protein leakage into the alveolar space. Hyperoxia increased SP-B messenger RNA (mRNA) and total protein concentrations by 2-fold in SP-B+/+ and SP-B+/- mice, but decreased the abundance of SP-B protein in lavage fluid relative to total protein only in SP-B+/- mice. Hyperoxia increased SP-B expression, but apparently not enough to maintain SP-B function and lung compliance in the presence of increased protein leakage in SP-B+/- mice. Increased alveolar-capillary leakage and relative deficiency of SP-B may therefore contribute to oxygen-induced pulmonary dysfunction in SP-B+/- mice. These data support the concept that SP-B plays an important protective role in the lung.
|Number of pages||10|
|Journal||American Journal of Respiratory Cell and Molecular Biology|
|Publication status||Published - 1999|
ASJC Scopus subject areas
- Cell Biology
- Molecular Biology
- Pulmonary and Respiratory Medicine