Mice with different histocompatibility alleles in otherwise identical backgrounds (congenic inbred strains of H-2a and H-2b haplotypes), were used to study the possible influence of the major histocompatibility complex (MHC) upon glucocorticoid-stimulated pulmonary surfactant synthesis during embryonic and fetal stages of mouse lung development. Pregnant C57BL/10SnJ (H-2b) and congenic B10.A/SnSgJ (H-2a) mice were administered single or consecutive intraperitoneal injections of betamethasone during the period of 14 through 17 days gestation. Assays for incorporation of [3H]choline into total lipid and saturated phosphatidylcholine (an index for pulmonary surfactant synthesis) were conducted, 24 hr following the last treatment, on Days 17 or 18 of gestation. Control mice received injections of phosphate-buffered saline. The H-2 genotype appears to influence the relative responsiveness of glucocorticoid-stimulated surfactant synthesis during fetal lung development. The B10.A strain (H-2a haplotype) was more responsive to glucocorticoid-stimulated pulmonary surfactant synthesis than the H-2b haplotype. Whereas both strains were responsive to glucocorticoid-stimulated [3H]choline incorporation into lung surfactant, the differences in responsiveness at specific fetal stages suggest that genes within or closely linked to the H-2 complex might have a role in pulmonary surfactant biosynthesis during mouse lung development. The results also suggest the possibility that relative susceptibility to congenital pulmonary disorders may be influenced by the H-2 complex.
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