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Alkylglycerols (AG) arc glyceryl ether lipids and are present in human and cow's milk and the hematopoietic organs such as bone marrow, spleen, and liver. The biologic effects of AG include stimulation of blood leukocyte and thrombocyte production and activation of macrophage and anti-tumor activity. The present study was conducted to determine the effects of dietary AG in lactating rats on AG levels in milk and development of certain immune responses in the pups. Lactating rats were fed diets supplemented with various levels of AG. Milk samples were expressed from the dams and blood was collected from the pups on postpartum d 8, 16, and 24. Concentrations of AG in milk from the dams fed AG were significantly greater than those of the controls @ < 0.05). Peripheral blood granulocytes were significantly elevated in pups from the dams fed AG, but there were no differences in peripheral blood lymphocyte numbers. Plasma levels of immunoglobulins were significantly greater for IgG @ < 0.01) and IgM @ < 0.001) in pups from the dams fed AG than in the control pups. The supplementation of AG in the diets of lactating dams significantly elevated AG levels in the milk, and the increased AG in the milk subsequently stimulated certain immune responses in the pups. in the newborn depends on the prompt and precise integration of cellular and humoral immune responses. The fetus has been in a sterile intrauterine environment, and at birth, the neonate has not yet developed a mature immune system (8). To deal with the hostile extrauterine environment, the newborn immune system must accomplish an adequate immunocompetence. Migliore-Samour

The mechanisms by which glucocorticosteroids promote osteoclastogenesis in vitro are uncertain. As macrophage colony-stimulating factor (MCSF) is critical for osteoclastogenesis, we hypothesized that glucocorticosteroids might regulate membrane-bound MCSF (mMCSF) and soluble MCSF (sMCSF) production by stromal cells or osteoblasts. ST2 cells or murine calvarial osteoblasts (MOBs) were treated with dexamethasone (Dex; 100 nM) and/or 1,25-dihydroxyvitamin D [1,25(OH)2D; 10 nM] for 3 days. Control values for mMCSF and sMCSF as units per 100,000 cells were 9 +/- 1.4 and 511 +/- 56 in ST2 cells and 5.9 +/- 0.8 and 379 +/- 47 in MOB cells, respectively. Dex increased mMCSF to 156 +/- 16% and 143 +/- 26% compared with the control value in ST2 and MOB cells, respectively, whereas 1,25-(OH)2D caused increases of 195 +/- 16% and 164 +/- 21%. In the presence of both Dex and 1,25-(OH)2D, mMCSF increased to 209 +/- 24% and 216 +/- 26% in the two cell types, respectively. 1,25-(OH)2D caused modest increases in sMCSF, as expected, in both cell types (153 +/- 6% and 122 +/- 4%). Dex inhibited 1,25-(OH)2D-stimulated sMCSF (115 +/- 7% of control) in ST2 cells. Analysis of mMCSF transcript levels by semiquantitative RT-PCR revealed Dex-stimulated increases of 170 +/- 11% in ST2 cells and 126 +/- 16% in MOB cells compared with the control level. The increased expression of the transcript for sMCSF in the presence of Dex and 1,25-(OH)2D, measured by both RT-PCR and Northern analysis (219 +/- 53% and 242%, respectively), despite inhibition of sMCSF protein, indicated that the inhibitory effect of Dex in ST2 cells was posttranscriptional. Half-life studies showed that Dex prolonged MCSF messenger RNA from 2.8 to 7.5 h. These results suggest that Dex influences osteoclastogenesis by increasing the expression of mMCSF by accessory cells in culture.