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At least 217 records · Page 12Linked to original sources
PubMed1989

Regulation of immunoglobulin production in hyperimmunoglobulin E recurrent-infection syndrome by interferon gamma.

The hyperimmunoglobulin E recurrent-infection (Job) syndrome (HIE) is a congenital disorder characterized by high serum IgE, chronic eczematoid dermatitis, and recurrent infections. We examined the effect of interferon gamma (IFN-gamma) on excessive IgE production in HIE patients. Spontaneous in vitro production of IgE by peripheral blood mononuclear cells from HIE patients was elevated compared to normal individuals and correlated with serum IgE. In 9 of 13 patients, IgE production by peripheral blood mononuclear cells was inhibited by 50% by IFN-gamma at 100-1000 units/ml, whereas inhibition by IFN-gamma at 10(4) units/ml ranged from 67 to 93% for these 9 patients. IFN-gamma also inhibited IgG1, IgG3, and IgG4 production by B lymphocytes without inhibiting IgG2 production. IFN-gamma was administered subcutaneously to 5 HIE patients. After 2 weeks of treatment with IFN-gamma (0.05 mg/m2) at three doses per week given on alternate days, peripheral blood mononuclear cells from all 5 HIE patients decreased spontaneous in vitro IgE production (27-62% decrease) with no change in IgG and IgM. One patient had a 58% decrease in serum IgE and another patient had a 50% decrease in serum IgE after the IFN-gamma was increased to 0.1 mg/m2 for three doses per week for a month. In both patients, serum IgE returned to pre-IFN-gamma-challenge levels 1-3 months after completion of treatment, and in vivo IFN-gamma did not affect serum IgG and IgM, although serum IgG4 decreased with changes in serum IgE. Our studies demonstrate that IFN-gamma can regulate production of IgE and some IgG subclasses in humans.

Antibody Formation↗
PubMed1982

Recurrent infection in the child.

In the child with recurrent infection, early recognition of defects in host defenses is critical for appropriate treatment and for patient survival and well-being. Familiarity on the physician's part with the clinical clues of an anatomic or functional defect can save time, money, and patient discomfort. When no such defect is apparent, the problem may be in the child's immunologic system and more specific testing is necessary to identify whether the defect is in cell-mediated immunity or is in the functioning of the phagocytic, complement, or humoral system. Treatments for these problems are available, but their success depends on early diagnosis before recurrent infection and malnutrition result in irreversible tissue damage.

Adolescent↗
PubMed2000

Inhaled particle-bound sulfate: effects on pulmonary inflammatory responses and alveolar macrophage function.

Acid sulfate-coated solid particles are a significant environmental hazard produced primarily by the combustion of fossil fuels. We have previously described a system for the nascent generation of carbonaceous particles surface coated with approximately 140 microg/m(3) acid sulfate [cpSO(4)(2-); 10 mg/m(3) carbon black (CB) and 10 ppm sulfur dioxide (SO(2)) at 85% relative humidity (RH)]. The effects of inhaled cpSO(4)(2-) on pulmonary host defenses are assessed in the present work. Mice were acutely exposed (4 h) to either 10 mg/m(3) CB, 10 ppm SO(2), or their combination at 10% or 85% RH in a nose-only inhalation chamber. No evidence of an inflammatory response was found following any of the exposures as assessed by total cell counts and differential cell counts from bronchoalveolar lavage fluid. However, alveolar macrophage Fc receptor-mediated phagocytosis decreased only following exposure to 140 microg cpSO(4)(2-), significant suppression occurred after 24 h, maximal suppression occurred at 3 days postexposure, and recovery to preexposure levels required 7-14 days. Intrapulmonary bactericidal activity (IBA) was also suppressed only after exposure to 140 microg cpSO(4)(2-); suppression was maximal at 1 day postexposure and recovered by day 7. To assess the effects of lower cpSO(4)(2-) concentrations, mice were repeatedly exposed to 1 mg/m(3) CB and 1 ppm SO(2) at 85% RH ( approximately 20 microg/m(3) cpSO(4)(2-) for 4 h/day) for up to 6 days. A significant decrement in IBA was observed following 5 and 6 days of exposure. These studies indicated that acute or repeated exposure to cpSO(4)(2-) could alter pulmonary host defense mechanisms.

Administration, Inhalation↗
PubMed1973

Iodinating ability of various leukocytes and their bactericidal activity.

A rapid method that employs monolayers of different phagocytic cells, primarily from guinea pigs and mice, has allowed a kinetic determination of (a) ingestion by these cells of labeled particles, (b) fixation of (131)I and (c) microbicidal activity in the cells after periods as short as 5' of exposure of bacteria to phagocytes. Phagocytes so examined included polymorphonuclear leukocytes (PMN) elicited into the peritoneal cavity, elicited peritoneal mononuclear cells (monocytes) (MN), and peritoneal macrophages (MAC) obtained simply by lavage. Circulating PMN from normal human subjects and from children afflicted with chronic granulomatous disease were also studied. The potential for generation of H(2)O(2) (a key component of the iodinating system) of all the normal cells studied, gauged by their content of cyanide-insensitive NADH oxidase, seemed comparable. Peroxidase levels varied widely, and were highest in PMN and almost undetectable in MAC. Catalase was at negligible levels in all the cell types obtained from mice. The fixation of (131)I by phagocytes ingesting (14)C-labeled dead tubercle bacilli appeared to be primarily a function of the cellular peroxidase content. Thus, mouse macrophages, with virtually no peroxidase, displayed no fixation of iodide. PMN proved far more able to fix (131)I during phagocytosis than did MN. In experiments comparing PMN from normal human subjects and from children with chronic granulomatous disease (CGD), a sex-linked condition characterized by a deficiency of H(2)O(2) production during phagocytosis and low microbicidal activity, the iodination ratio of CGD cells was dramatically less than that of normal PMN (by about two orders of magnitude). Capacity for iodination was correlated with bactericidal activity toward E. coli. At low bacterial loads (ca. 5:1), phagocytes killed efficiently, and little discrepancy in ability among cell types was apparent. Under the stress of higher loads of (14)C-labeled E. coli (ca. 100:1), differences in bactericidal activity were exaggerated, and a substantial disparity between MN and PMN was observed in favor of the latter. The hierarchy for killing efficiencies therefore agreed with that for iodination, with one notable exception: mouse MAC were consistently competent in their killing activity, more so than MN, even though they virtually lack peroxidase and the ability to iodinate ingested bacteria.

Animals↗
PubMed1978

Granulomatous hepatitis and pleuritis after ileal bypass for obesity.

A patient is presented who developed a granulomatous hepatitis and pleuritis approximately 7 months after an ileal bypass procedure for morbid obesity. Although the etiological agent was presumed to be Mycobacterium tuberculosis no pathogenic organism was grown from the liver, pleura, bone marrow, sputum, or gastric aspirate. The possibly increased susceptibility of these patients to mycobacterial infections is discussed. The value of obtaining serum levels of ethambutol, isoniazid, and rifampin, in patients with malabsorption is stressed. Although this patient seemed to respond to antituberculous therapy, other possible causes for the granulomatous process are explored.

Ethambutol↗
PubMed1975

Intracellular bactericidal activity of leukocytes in whole blood for the diagnosis of chronic granulomatous disease of childhood.

A simplified method for the assay fo intracellular bactericidal activity of leukocytes in whole blood was developed. Providing that serum-resistant organisms are studied, the method can be used with gram-negative baccilli as well as with Staphylococcus aureus. The abnormalities characteristic of patients with chronic granulomatous disease of childhood and their mothers can be readily detected by this technique. By this means an abnormality in intracellular killing of Pseudomonas cepacia in a patient with chronic granulomatous disease and in his heterozygotic mother was found.

Benzenesulfonates↗
PubMed1980

Response of plasma fibronectin to major body burn.

The ability of macrophages of phagocytize particulate matter is largely dependent on fibronectin, a nonspecific opsonin found in plasma. Fibronectin depletion, resulting in reticuloendothelial system (RES) depression, occurs following a variety of physical insults. RES depression may contribute to postinjury sequelae such as respiratory distress syndrome and septicemia. Fibronectin concentration was measured in the plasma of sheep with chronic lung lymph fistulas subjected to controlled thermal injury. Fibronectin levels were significantly (p < 0.05) decreased at 4, 24, 48, and 72 hours following burning. Fibronectin concentration decreased in parallel with serum albumin concentration; serum globulin concentrations did not decrease. Fibronectin concentration had an inverse relationship to lung lymph flow, a reflection of pulmonary transvascular fluid filtration rate. The role of fibronectin in the pathogenesis of postinjury respiratory distress syndrome deserves further exploration.

Adult↗
PubMed1986

The acridine orange fluorochrome microassay: a new technique for quantitation of neutrophil function in burned patients.

A new assay for determination of neutrophil bacterial killing and phagocytosis is presented. The acridine orange (AO) fluorochrome microassay is a simple, reliable technique for assessing polymorphonuclear (PMN) function. It requires small amounts of blood and provides a rapid and reproducible quantitation of neutrophil activity. Using this technique, bacterial killing and phagocytosis were assessed in a group of five severely burned patients admitted to the Medical College of Virginia Burn Unit. All patients studied demonstrated a significant decrease in bacterial killing at some point during their clinical course. The AO assay was found to be a reliable and effective means of quantitating PMN bacterial phagocytosis and killing in this group of burned patients.

Acridine Orange↗
PubMed1983

The hyperimmunoglobulin E recurrent-infection (Job's) syndrome. A review of the NIH experience and the literature.

The hyperimmunoglobulin E recurrent-infection syndrome (HIE) entails a disorder of recurrent bacterial infections of the skin and sinopulmonary tract commencing in infancy or early childhood in the presence of serum levels of IgE which are at least 10 times normal (greater than 2,000 IU/ml). Variable concomitants of HIE are coarse facies, chronic eczematoid rashes, cold cutaneous abscesses, mild eosinophilia, mucocutaneous candidiasis, and a neutrophil chemotactic defect. The bacteria which commonly infect these patients are Staphylococcus aureus and Haemophilus influenzae although Streptococcus pneumoniae and enteric gram-negative rods are seen in some cases. Other than pneumonias, deep-seated infections are unusual, although osteomyelitis, arthritis, and visceral abscesses are seen. Bacteremia and sepsis are rare. Therapy should involve prolonged intravenous antibiotics and early surgery to treat infections which usually seem deceptively benign. HIE patients' neutrophils display a variable chemotactic defect, and their mononuclear cells variably produce an inhibitor of neutrophil chemotaxis. The production of the inhibitor correlates with the in vitro chemotactic defect. The basis of the propensity for recurrent infections is still speculative, and the further study of this syndrome should add new dimensions to our understanding of host defenses against bacterial invaders.

Abscess↗
PubMed2001

Granulocyte function disorders: aspects of development, genetics and management.

The field of phagocytic disorders has attained major biologic and clinical significance in the past 40 years. The development of exciting new techniques in molecular biology and the cellular physiology of signal transduction have made it possible to identify the genetic defects involved in many of these disorders. Moreover through immunopharmacologic intervention, bone marrow or peripheral or cord blood stem cell transplantation along with the prospect of gene therapy, we have begun attempts to at least partially correct genetic defects in cell development and activation pathways in the entire spectrum of phagocyte disorders. Carrier detection and prenatal diagnosis employing with chain reaction techniques or direct nucleotide sequencing in fetal blood have made these diseases potentially preventable or treatable in utero or shortly after birth.

Agranulocytosis↗