The Resource Mothers Study of Maternal Phenylketonuria: preliminary findings.

Women with phenylketonuria (PKU) must follow a strict low-phenylalanine diet during pregnancy in order to protect the fetus from the deleterious effects of high maternal blood phenylalanine. The Resource Mothers Study of Maternal PKU was undertaken to determine whether a home visitation programme was effective in helping women with PKU attain blood phenylalanine control earlier during pregnancy. Resource Mothers were trained to provide social support and practical assistance to women with PKU during pregnancy. Eight metabolic clinics in the United States participated in the study. Women with PKU who were planning pregnancy or already pregnant were enrolled in the study and were treated with a low-phenylalanine diet aimed at controlling blood phenylalanine to 120-360 micromol/L. They were randomly assigned to receive the services of a Resource Mother (RM group) or to a control group. Fifty women were enrolled, and accounted for 44 pregnancies which resulted in 28 live births, and 6 spontaneous abortions. Ten women are currently pregnant and another 6 have not become pregnant. Fifty-six percent of enrolled women began the diet prior to becoming pregnant. Fifty-three percent of women in the Resource Mother group were in metabolic control by 10 weeks gestation as compared to 39% in the control group. In addition, women who began diet after pregnancy and had a Resource Mother attained metabolic control earlier (mean gestational age of 22.4 weeks in the RM group vs 29.8 weeks in the control group). There was no difference in birth measurement z -scores of offspring born to women in the RM group compared to controls. All but 4 women rated themselves as feeling worse about the diet at the end of pregnancy than at the beginning, and few women in either group remained on diet after delivery.

Human lung lavage surfactant enhances staphylococcal phagocytosis by alveolar macrophages.

We tested the effect of a preparation of human lung lavage surfactant (SAM) on phagocytosis and intracellular killing of Staphylococcus aureus by human alveolar macrophages (AM). When staphylococci were incubated with 100 to 300 micrograms of SAM, AM phagocytosis but not intracellular killing efficiency was enhanced. The mean numbers of intracellular staphylococci/AM were 36.0 +/- 2.7 and 23.3 +/- 2.8 in the SAM and control groups, respectively (p less than 0.001). The AM intracellular killing efficiency was 40.9 +/- 3.3% and 39.5 +/- 3.9% in the SAM and control groups, respectively (p greater than 0.05). Our results suggest that SAM is an important nonimmune opsonin for bacterial phagocytosis by human AM.

Functional heterogeneity of isopycnic fractions of rat alveolar macrophages.

Rat alveolar macrophages separated into four isopycnic fractions on Percoll gradients were functionally heterogeneous in bacterial phagocytosis, intracellular killing, superoxide anion release, and lysosomal enzyme activity but not in hydrogen peroxide release. With increasing alveolar macrophage density, phagocytosis, intracellular killing, superoxide anion release, and lysozyme activity increase, and acid hydrolase activity decreases.

Rat lung lavage surfactant enhances bacterial phagocytosis and intracellular killing by alveolar macrophages.

We have tested the effect of a preparation of rat lung lavage surfactant (SAM) on phagocytosis and intracellular killing of Staphylococcus aureus by rat alveolar macrophages (AMs). The SAM was isolated and purified by density gradient centrifugation. It was highly enriched in disaturated phosphatidylcholine, and invariably lowered the surface tension of a clean saline solution to less than 10 dynes/cm at 37 degrees C. We used a radiometric assay to measure phagocytosis as uptake by AMs of 14C phenylalanine labelled staphylococci, and intracellular killing as incorporation of 3H thymidine by viable staphylococci from the lysed AMs. When staphylococci were incubated with 100 to 300 micrograms of SAM, both phagocytosis and intracellular killing efficiency were enhanced. The mean numbers of intracellular staphylococci/AM were 24.3 +/- 3.8 and 18.3 +/- 3.0 in the SAM and control groups, respectively (p less than 0.001). The mean intracellular killing efficiency was 59.6 +/- 6.76% and 39.7 +/- 7.17% in the SAM and control groups, respectively (p less than 0.001). Previous studies have shown that unpurified rat lung lavage fluid enhances intracellular killing of staphylococci by AMs. Our results suggest that SAM may be the active principle in lung lavage fluid that enhances intracellular killing. In addition, in our test system, SAM enhanced staphylococcal phagocytosis by AMs.