| First Author | Tokieda K | Year | 1999 |
| Journal | Am J Respir Cell Mol Biol | Volume | 21 |
| Issue | 4 | Pages | 463-72 |
| PubMed ID | 10502556 | Mgi Jnum | J:59460 |
| Mgi Id | MGI:1351695 | Doi | 10.1165/ajrcmb.21.4.3436 |
| Citation | Tokieda K, et al. (1999) Surfactant protein-B-deficient mice are susceptible to hyperoxic lung injury [see comments]. Am J Respir Cell Mol Biol 21(4):463-72 |
| abstractText | Surfactant protein-B (SP-B) is a small, hydrophobic peptide 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. |
