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PubMed1983

Systemic lupus erythematosus in Staphylococcus aureus hyperimmunoglobulinaemia E syndrome.

The prevalence of autoimmune diseases, including systemic lupus erythematosus, is increased in failure of certain host defence mechanisms. Systemic lupus erythematosus, however, has not been recorded as a late complication of the Staphylococcus aureus hyperimmunoglobulinaemia E (hyper-IgE) syndrome. Such a case was investigated in a man suffering from a classic example of the syndrome. Antinuclear antibodies were analysed on a molecular basis. The emergence of immunological and clinical features of systemic lupus erythematosus in patients with defective host defence mechanisms against staphylococcal infections is unlikely to be fortuitous and may help elucidate the pathogenesis of systemic lupus erythematosus. The observations will also aid the long term management of patients with S aureus hyper-IgE syndrome.

Adult↗
PubMed1986

Ileocecal histoplasmosis mimicking Crohn's disease in a patient with Job's syndrome.

A 16-years-old male with a history of Job's syndrome and a recent diagnosis of Crohn's disease was admitted to the hospital because of abdominal pain, nonbloody diarrhea, weakness, and fever. Due to failure to respond to medical therapy it was decided that an operation was indicated, and resection of the terminal ileum and right colon was performed. Cecum and ileum were inflamed, and pathologic studies revealed the presence of budding yeasts which on special stain were diagnostic of Histoplasma species. Successful management was accomplished with oral ketoconazole.

Adolescent↗
PubMed1979

Myeloperoxidase activity and bactericidal function of PMN in iron deficiency.

In children with iron deficiency anemia, bactericidal capacity of polymorphonuclear leukocytes (PMN) and serum opsonic activity were studied. Nitroblue tetrazolium test (NBT), hexose monophosphate (HMP) shunt activation, and myeloperoxidase (MPO) activity of PMN of these cases were also examined. Bactericidal capacity and HMP shunt activation were found to be decreased in iron deficiency anemia ( p less than 0.001). MPO activity, NBT test, and serum opsonic activity were found to be within normal limits. After 1 1/2 months of iron therapy there was an improvement in bactericidal capacity and it returned to a normal level after 3 months of therapy.

Adolescent↗
PubMed1976

Vascular lesion (arteriovenous aneurysm or haemangioma) of the orbit in a case of chronic granulomatous disease.

A case of arteriovenous aneurysm or congenital arteriovenous haemangioma of the orbit is described in a 5-year-old boy with chronic granulomatous disease. Lipid pigments are demonstrated in endothelial cells as well as in histiocytes and fibrocytes. There appears to be a decreased ability to remove phagocytosed haemosiderin, in addition to the well-known inability of granulocytes, and probably to some extent of histiocytes, to kill phagocytosed bacteria.

Arteriovenous Malformations↗
PubMed1972

Abnormal bactericidal, metabolic, and lysosomal functions of Chediak-Higashi Syndrome leukocytes.

Phagocytic, antimicrobial, and metabolic functions were studied in leukocytes obtained from three patients with the Chediak-Higashi syndrome (CHS) and compared to normals, individuals, heterozygous for Chediak-Higashi syndrome, and two subjects with chronic granulomatous disease of childhood (CGD). Chediak-Higashi syndrome leukocytes showed normal ingestion of a variety of bacteria, Candida albicans, and polystyrene latex particles. Intracellular destruction was significantly impaired for Staphylococcus aureus, Group D streptococci, and a rough strain of Type II pneumococci over a 2 hr incubation. Killing of Serattia marcescens was consistently delayed at 1 hr whereas that of Escherichia coli and C. albicans appeared normal, unless the incubations were shortened to 20 min. Examination of the rates of killing indicated that the greatest defect occurred in the first 20 min of contact between Chediak-Higashi syndrome cells and bacteria. Separation of Chediak-Higashi syndrome granulocytes from monocytes revealed that the former were most defective in bactericidal activity. After phagocytosis, Chediak-Higashi syndrome granulocytes displayed a normal burst in oxygen consumption and oxidation of glucose-1-(14)C and glucose-6-(14)C and formate-(14)C. Oxidation of glucose-1-(14)C by non-phagocytizing Chediak-Higashi syndrome granulocytes and monocytes averaged 2-3 times normal, whereas glucose-6-(14)C and formate-(14)C oxidation were not significantly increased by resting cells. Iodination of intracellular protein by Chediak-Higashi syndrome leukocytes was significantly increased above normal in both the resting and phagocytizing state. Electron microscopic histochemistry revealed that almost all peroxidase activity was localized to the giant granules in Chediak-Higashi granulocytes, and after bacterial ingestion there was a failure of delivery of peroxidase to many phagosomes. Upon longer incubation more phagosomes acquired peroxidase activity, presumably through a fusion process, although many giant granules remained intact. The contrasting patterns and kinetics of the killing defects and the differing metabolic properties of Chediak-Higashi syndrome and chronic granulomatous disease leukocytes emphasize the pleiomorphic nature of inherited disorders of leukocyte function.

Adolescent↗
PubMed1972

Functional aspects of a second mechanism of candidacidal activity by human neutrophils.

We tested the ability of human neutrophils to kill five Candida species and the yeast Torulopsis glabrata. C. parapsilosis and C. pseudotropicalis were found to be killed readily by normal and myeloperoxidase-deficient neutrophils and were selected to probe the myeloperoxidase-independent fungicidal mechanisms of the neutrophil. These organisms were killed with relatively normal (C. parapsilosis) or moderately reduced (C. pseudotropicalis) effectiveness by neutrophils from two boys with X-linked chronic granulomatous disease. Azide (2 mm) and sulfadiazine (4 mm) exerted a relatively small inhibitory effect on the ability of normal neutrophils to kill C. parapsilosis. These compounds did not, however, inhibit the killing of C. parapsilosis by myeloperoxidase-deficient neutrophils, although they blocked their iodination of ingested Candida cells. Anaerobic incubation conditions inhibited the ability of normal neutrophils to kill C. parapsilosis slightly but did not impair this function in myeloperoxidase-deficient cells. All of the Candida species tested had catalase activity, yet their sensitivity to H(2)O(2) in cell-free systems varied considerably. Our C. parapsilosis strain was extraordinarily resistant to H(2)O(2) (LD(75): 0.14 m), as compared with C. pseudotropicalis or with our reference strain of C. albicans (LD(75): 2.3 x 10(-3)m and 3.4 x 10(-3)m, respectively). These data establish the existence in human neutrophils of a second mechanism that exerts microbicidal activity against certain Candida species; the mechanism is unrelated to myeloperoxidase, iodination, or to the direct effects of H(2)O(2) generated by the endogenous metabolic processes of the neutrophil. As yet unidentified, this mechanism appears to remain operative in the neutrophils of subjects with hereditary myeloperoxidase deficiency or chronic granulomatous disease.

Aerobiosis↗
PubMed1973

Degradation of thyroid hormones by phagocytosing human leukocytes.

Thyroxine (T(4)) and triiodothyronine (T(9)) are rapidly degraded by a purified preparation of myeloperoxidase (MPO) and H(2)O(2) with the formation of iodide and material which remains at the origin on paper chromatography. Deiodination by MPO and H(2)O(2) occurs more readily at pH 7.0 than at pH 5.0 in contrast to iodination by this system which is known to occur more readily at pH 5.0 than at pH 7.0. Degradation is inhibited by azide, cyanide, ascorbic acid, and propylthiouracil. Methimazole stimulates deiodination by MPO and H(2)O(2) but inhibits this reaction when MPO is replaced by lactoperoxidase or horseradish peroxidase.Intact human leukocytes, in the resting state, degrade T(4) and T(3) slowly: degradation, however, is increased markedly during phagocytosis of preopsonized particles. Serum inhibits this reaction. T(3) can be detected as a minor product of T(4) degradation. Proteolytic digestion of the reaction products increases the recovery of monoiodotyrosine. The fixation of iodine in the cytoplasm of leukocytes which contain ingested bacteria was detected radioautographically. Chronic granulomatous disease leukocytes, which are deficient in H(2)O(2) formation, degrade T(4) and T(3) poorly during phagocytosis. MPO-deficient leukocytes degrade the thyroid hormones at a slower rate than do normal leukocytes although considerable degradation is still observed. Azide, cyanide, ascorbic acid, and propylthiouracil which inhibit certain peroxidasecatalyzed reactions inhibit degradation by normal leukocytes; however, inhibition is incomplete. Formation of iodinated origin material is inhibited to a greater degree by azide, cyanide, and propylthiouracil than is deiodination. Methimazole inhibits the formation of iodinated origin material by both normal and MPO-deficient leukocytes. However, deiodination by normal leukocytes is stimulated and that of MPO-deficient leukocytes is unaffected by methimazole. Hypoxia inhibits the degradation of T(4) and T(3) by untreated normal or MPO-deficient leukocytes and by normal leukocytes treated with azide or methimazole. These data suggest that both MPO-dependent and MPO-independent systems are involved in the degradation of T(4) and T(3) by phagocytosing leukocytes. The role of leukocytic degradation of T(4) and T(3) in thyroid hormone economy and in leukocytic microbicidal activity is considered.

Ascorbic Acid↗
PubMed1973

Metabolism of L-thyroxine by phagocytosing human leukocytes.

Intact normal human leukocytes deiodinated L-thyroxine (T(4)) with the generation of inorganic iodide, chromatographically immobile origin material, and small quantities of L-triiodothyronine (T(3)). When phagocytosis was induced in the leukocytes through the addition of zymosan particles that had been opsonized by coating with plasma, T(4)-deiodination was greatly stimulated. In addition to the stimulation of T(4)-deiodination, the accumulation by the leukocytes of undegraded T(4) was increased. Anoxia, which has previously been shown not to interfere with phagocytosis, did not prevent the increased cellular accumulation of T(4) that phagocytosis induced, but virtually abolished T(4)-deiodination. On the other hand, calcium, which has previously been shown to be required for optimal phagocytosis, was required for the increase in both the cellular accumulation and deiodination of T(4) that phagocytosis induced. Phospholipase-C, which has previously been shown to induce a metabolic burst that mimics that induced by phagocytosis, did not increase the cellular accumulation or deiodination of T(4). On the other hand, colchicine, which has previously been shown to depress the metabolic burst that accompanies phagocytosis, did not prevent the increase in either the cellular accumulation or deiodination of T(4) that phagocytosis induced. Thus, increased accumulation of T(4) by the leukocytes during phagocytosis appears to be the primary factor responsible for the stimulation of deiodination that phagocytosis induces. The increased accumulation of T(4) did not appear to be owing to engulfment of suspending medium surrounding the particles or to binding of T(4) to the particles themselves. In addition to the enhanced cellular accumulation, other factors related to the metabolic burst that accompanies phagocytosis might also be involved in the stimulation of T(4)-deiodination. In leukocytes from two patients with chronic granulomatous disease, a disorder in which phagocytosis appears to occur normally but in which the metabolic burst and attendant increase in hydrogen peroxide generation do not occur, stimulation of T(4)-deiodination was either greatly diminished or totally lacking. In myeloperoxidase-deficient leukocytes, on the other hand, stimulation of T(4)-deiodination was at least as great as that in normal cells. Thus, we conclude that the primary factor responsible for the increased deiodination of T(4) that phagocytosis induces is the enhanced cellular uptake of hormone. The increased generation of hydrogen peroxide that accompanies phagocytosis may be necessary for the enhanced deiodination of the accumulated T(4), but the latter reaction does not require the mediation of myeloperoxidase.

Calcium↗
PubMed1974

Effects of phorbol myristate acetate on the metabolism and ultrastructure of neutrophils in chronic granulomatous disease.

Previous investigations have demonstrated that phorbol myristate acetate (PMA), the active principle of croton oil, stimulates alterations in normal polymorphonuclear leukocytes (PMN) that resemble closely the changes that develop in the cells after phagocytosis of bacteria. The present study has compared the effects of PMA and heat-killed bacteria on the oxygen uptake, glucose oxidation, nitroblue tetrazolium (NBT) reduction, and ultrastructure of normal neutrophils and PMN from six patients with chronic granulomatous disease (CGD). PMA stimulated oxygen consumption, hexose monophosphate shunt activity, and NBT reduction in normal cells but failed to produce similar effects in CGD neutrophils. However, PMA did induce formation of cytoplasmic vacuoles in the CGD cells similar to those observed in normal neutrophils. The results indicate that PMA is a useful nonparticulate agent for distinguishing between normal and CGD neutrophils and for studying basic mechanisms of phagocytosis in normal and abnormal PMN.

Alcohols↗
PubMed1975

NADPH oxidase deficiency in X-linked chronic granulomatous disease.

We measured the cyanide-insensitive pyridine nucleotide oxidase activity of fractionated resting and phagocytic neutrophils from 11 normal donors, 1 patient with hereditary deficiency of myeloperoxidase, and 7 patients with X-linked chronic granulomatous disease (CGD). When measured under optimal conditions (at pH 5.5 and in the presence of 0.5 mM Mn++), NADPH oxidase activity increased fourfold with phagocytosis and was six-fold higher than with NADH. Phagocytic neutrophils from patients with CGD were markedly deficient in NADPH oxidase activity.

Adolescent↗