Brief exposure to 95% oxygen alters surfactant protein D and mRNA in adultrat alveolar and bronchiolar epithelium

Citation
Ao. Aderibigbe et al., Brief exposure to 95% oxygen alters surfactant protein D and mRNA in adultrat alveolar and bronchiolar epithelium, AM J RESP C, 20(2), 1999, pp. 219-227
Citations number
52
Categorie Soggetti
da verificare
Journal title
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
ISSN journal
10441549 → ACNP
Volume
20
Issue
2
Year of publication
1999
Pages
219 - 227
Database
ISI
SICI code
1044-1549(199902)20:2<219:BET9OA>2.0.ZU;2-N
Abstract
Surfactant protein D (SP-D), which has structural homology to C-type lectin binding regions, may play a role in host defense and has no known surfacta nt function. Because other surfactant proteins have been shown to be increa sed after prolonged periods of hyperoxia, we sought to evaluate the early e ffects of hyperoxia (95% O-2) on expression of SP-D in the adult male rat l ung. Animals were exposed to air or to 12, 36, or 60 h of 95% O-2. Northern blot analysis of total lung RNA revealed marked SP-D mRNA increases at 12 h 95% O-2 compared with air-exposed controls, with decreasing expression to near that of ail-exposed animals by 60 h. Semiquantitative in situ RNA hyb ridization demonstrated parallel results, with increased numbers of labeled alveolar epithelial (AE) and bronchiolar epithelial (BE) cells at 12 h and increased intensity of labeled alveolar cells, compared with air-exposed c ontrols. After 60 h of exposure to 95% O-2, mRNA label intensity in AE and BE was decreased to levels near those seen in air-exposed animals. In contr ast, Western blotting showed a decline in total lung SP-D with 95% O-2 expo sure, beginning at 12 h and continuing at 36 and 60 h, respectively. Semiqu antitative immunohistochemistry demonstrated a decline in AE labeling paral lel to the total lung Western blot results, but labeled total BE cell numbe rs increased (P = 0.10). Hyperoxia had differential effects on SP-D abundan ce in AE and BE cells, and therefore may influence the availability of SP-D to bind microbial pathogens in the airways depending on cell type and loca tion.