Increased Reactive Oxygen Species Production by Peripheral Blood Mononuclear Leukocytes, not by Polymorphonuclear Leukocytes, in Atopic Dermatitis / 소아알레르기및호흡기학회지

PURPOSE: Reactive oxygen species (ROS) are known as a potential mediators that sustain chronic inflammation in atopic dermatitis (AD). To determine the role of peripheral blood mononuclear leukocytes (MO) and polymorphonuclear leukocytes (PMN) in prolonged inflammation, ROS generation of those cells in AD was examined. METHODS: Seventeen AD patients and 10 healthy controls were enrolled. MO and PMN were stimulated with the reagents: phobol ester (PMA), adenosine triphosphate (ATP), and chemotactic peptide (f-MLP). ROS levels were measured using chemiluminescence assay. RESULTS: In AD, chemiluminescence response of unstimulated MO was higher than that of normal controls. MO from AD patients produced 1.58-1.80 higher ROS for up to 30 minutes than the controls. When the cells were treated with the reagents (PMA, ATP, f-MLP), all the stimuli enhanced chemiluminescence activity of MO. When MO were treated with PMA, the ratio of ROS produced by MO of patients to that of the controls decreased. When the cells were treated with either ATP or f-MLP, the quantity of ROS generated by MO from the controls was greater than the controls. PMN from both AD patients and the controls generated ROS for 30 min similarly. As treated with the reagents, PMN from AD patients produced a smaller ROS than the controls. CONCLUSION: These results indicate MO but not PMN from AD patients were primed and ready for activation in vivo, and a reduced function of PMN from AD patients was observed. In conclusion, enhanced respiratory burst activity of MO is implicated in the prolonged inflammation of AD.

The Activity of sICAM-1 and sVCAM-1 in Plasma of Preeclamptic Mother and Neonatal Cord Blood

PURPOSE: Current concepts of preeclampsia have been focused on dysfunction of the maternal vascular endothelium, a central pathogenetic feature of the disease. But it is uncertain whether maternal preeclampsia has a harmful effect on fetal or neonatal vascular endothelium. In this study, plasma levels of endothelial adhesion molecules in preeclamptic mother and cord blood were determined to delineate vascular effects of preeclampsia on neonates. METHOD: Quantitative determinations of sICAM-1 and sVCAM-1 were measured from plasma of preeclamptic mother and neonatal cord blood in pairs according to gestational age and was compared to nonpreeclamptic control groups. RESULTS: Plasma ICAM-1 level was significantly higher in the maternal groups compared to corresponding cord groups (P<0.001). Preeclamptic maternal groups showed significantly higher sICAM-1 level compared to control maternal groups (P<0.001) and preterm maternal groups showed higher levels than term maternal groups (P<0.001). The level of sICAM-1 was significantly elevated in preeclamptic preterm cord groups than other cord groups (P<0.001). In respect to plasma sVCAM-1 level, higher value was observed in the preeclamptic preterm cord groups than preeclamptic preterm maternal groups. CONCLUSIONS: Elevation of the plasma sICAM-1 level caused by factors including vascular endotherial damage in preeclamptic mothers was observed in their neonates but with much lesser degree than their mothers. Factors associated with preterm labor other than maternal preeclampsia may seem to influence vascular endothelial injury in the cord blood.

Plasma G-CSF and GM-CSF Concentrations and Expression of their Receptors on the Granulocyte in Children with Leukocytosis

PURPOSE: Granulocyte-colony stimulating factor(G-CSF) and granulocyte macrophage-colony stimulating factor(GM-CSF) are principal cytokines in granulopoiesis and their physiologic effects are mediated through binding to specific cell surface receptors. Although it is known that the level of serum G-CSF and GM-CSF, and presentation of the receptors are increased in infectious diseases, there have been no studies to find the correlation between the granulopoiesis and leukocytosis. This study was designed to measure G-CSF and GM-CSF in leukocytosis and in control and to demonstrate the possible pathogenesis of granulopoiesis in leukocytosis using quantitative analysis of G- CSF, GM-CSF and their CSFr. METHODS: The plasma levels of G-CSF, GM-CSF of 13 children without leukocytosis and 14 children with leukocytosis were measured. Counts of cell surface G-CSFr and GM-CSFr were measured by combining anti G-CSFr and anti GM-CSFr monoclonal antibodies to their respective receptors by using quantitative flow cytometric assay. RESULTS: There was no significant difference betweeen the plasma concentration of G-CSF and GM-CSF in acute leukocytosis and in the control group. However, levels of G-CSFr in acute leukocytosis decreased significantly compared to the control(P=0.012) and the levels of GM-CSFr in both groups revealed no significant difference. CONCLUSION: Increase in the number of leukocyte in leukocytosis was mediated by increasing the number of neutrophil, and increased plasma concentration of G-CSF may be the cause of neutrophilia. But GM-CSF did not have any influence on leukocytosis.