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The influence of ethylenediamine-tetra-acetate (EDTA, 10(-3) M, 10(-5) M and 10(-7) M), sodium iodoacetate (CH2 . I. COONa, 10(-4) M and 10(-6) M) and potassium cyanide (KCN, 10(-2) M, 10(-3) M and 10(-5) M) on the release of cobalophilins (vitamin B12 binding proteins) from polymorphonuclear granulocoytes (PMN) was studied. The agents mentioned above reduced the release of cobalophilins from resting and functionally stimulated granulocytes. This effect increased with the growth of concentration of these agents in the sample. The inhibitory effect of EDTA, CH2 . I. COONa and KCN on phagocytosis-activated cobalophilins release occurred irrespective of the time of granulocytes stimulation. This could be observed in these experiments, where granulocytes were first affected by these chemical agents and then stimulated functionally, as well as in those samples where EDTA, CH2 . I . COONa, and KCN influenced the cells after incubation with latex particles. The inhibitory effect of EDTA was diminished in the presence of a higher concentration of calcium ions in an incubation medium. On the contrary, CH2 . I . COONa reduced the release of cobalophilins from PMN during phagocytosis irrespective of the concentration of calcium ions in the medium.
The studies have evaluated the effect of methotrexate and vincristine on the release of cobalophilins (vitamin B12 binding proteins) from resting and functionally stimulated polymorphonuclear granulocytes (PMN). Methotrexate (2.5 micrograms/ml; 5.0 micrograms/ml; 20.0 micrograms/ml; and 50.0 micrograms/ml) and vincristine (0.3 microgram/ml; 0.6 microgram/ml; 2.4 micrograms/ml; and 6.0 micrograms/ml) inhibited the cobalophilins release from resting granulocytes. This effect increased with growing concentrations of these drugs. Stimulated PMN could be shown to release cobalophilins more actively than resting granulocytes. Methotrexate (2.5 micrograms/ml; 5.0 micrograms/ml and 20.0 micrograms/ml) and vincristine (0.3 microgram/ml; 0.6 microgram/ml and 2.4 micrograms/ml) inhibited the phagocytosis-activated release of cobalophilins irrespective of the time of PMN stimulation, i.e. before or after being incubated with latex particles.
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There are two ways to find the cause of primary immunodeficiency diseases. One approach is to start with the immune defect and work backwards, using in vitro techniques to define where the primary abnormality lies in the immune response. Immunologists favour this approach for obvious reasons; and it is not without virtue since, for example, it has shown that the defect in most cases of primary hypogammaglobulinaemia is due to a failure of B lymphocyte maturation. The alternative approach is to screen empirically for defects in biochemical pathways in the hope of finding a clue which will eventually lead to the underlying disorder. This is a sensible approach in diseases which are clearly inherited (e.g. X-linked hypogammaglobulinaemia) but is less attractive in a disease such as late onset hypogammaglobulinaemia which is not obviously inherited. In practice, such procedures involve screening the urine for abnormalities in the quality or quantity of excreted compounds. Another way is to screen for abnormalities in organelle integrity by measuring the activity of various enzymes in subcellular fractions. In reality, the clue to the metabolic defect is usually discovered by accident, the prime example in our field being the discovery of adenosine deaminase (ADA) deficiency.
During the last decade, many biochemical and immunologic advances have been made in the treatment and understanding of sarcoidosis. These studies have helped us to understand the basic mechanisms involved in granuloma formation, and many clinicians have used the information to diagnose and assess the activity of sarcoidosis. Further studies are needed to clearly establish the role of these advances in the everyday management of patients with sarcoidosis.
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Human neutrophils were fractionated by nitrogen cavitation and Percoll density centrifugation, and the subcellular localization of FAD-flavoprotein, b-cytochrome, NADH-cytochrome b5 reductase, and NADPH-dependent cytochrome c reductase were determined in normal cells, cells from two patients with chronic granulomatous disease (CGD), and normal cells that had been stimulated with phorbol myristate acetate. In normal cells, a FAD-flavoprotein is found in a 1:2 molar ratio, with cytochrome b in the fractions containing the specific granules. Triton X-114 phase distribution indicates that the b-cytochrome but not the b-cytochrome-associated flavoprotein is an integral membrane protein. 80% of this flavoprotein, as well as all the b-cytochrome, was absent in these fractions from 2 CGD patients, although these patients had normal quantities of FAD in the fractions containing plasma membranes and cytosol. During stimulation the b-cytochrome-associated flavoprotein of the granules translocates with the b-cytochrome to the plasma membrane where NADPH oxidase is localized. Definition of the role of these NADPH oxidase constituents may provide a molecular description of the normal neutrophil respiratory burst and the molecular defect(s) in CGD.
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