EXPRESSION AND DISTRIBUTION OF SURFACTANT PROTEINS AND LYSOZYME AFTERPROLONGED HYPERPNEA

We have induced prolonged hyperpnea in rats and examined the distribut ion of surfactant-associated proteins (SP-A and SP-B) and lysozyme in lamellar bodies (1b) and two alveolar fractions, one tubular myelin ri ch (alv-1) and the other tubular myelin poor (alv-2). We have also exa mined the expression of SP-A, SP-B, SP-C, and lysozyme mRNA in lung ti ssue and alveolar type II cells. Hyperpnea resulted in significant inc reases in 1b SP-A, lysozyme, and phospholipid (PL) but no change in th e protein-to-PL ratios, suggesting that 1b stoichiometry is constant. The SP-A- and SP-B-to-PL ratios were 33 and 18 times greater; respecti vely, in control alv-1 than in 1b, suggesting that alv-1 is enriched w ith these proteins. In contrast, the lysozyme-to-PL ratio was similar in control alv-1 and 1b. Hyperpnea did not alter the alv-1 SP-A- or SP -B-to-PL ratios, suggesting some constant stoichiometry to their lipid association; however, the lysozyme-to-PL ratio was reduced. Whereas h yperpnea significantly elevated the FL, SP-A, and lysozyme levels in a lv-2, the SP-B level was unchanged. We suggest that surfactant-associa ted lysozyme is secreted with 1b, the majority of SP-A is linked to li pid secretion but not necessarily with 1b, and the majority of SP-B se cretion is independent of PL secretion. Hyperpnea did not alter the mR NA expression of SP-A, SP-B, SP-C, or lysozyme in alveolar type II cel ls, but expression of SP-A and SP-B mRNA was significantly increased i n lung tissue.