Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been suggested that the IgE-dependent late-phase reaction to allergen exposure, with the features of an inflammatory cellular infiltration and airway hyperreactivity, is a link between anaphylaxis and continuous allergic airway disease. Our main knowledge of the cellular response to allergen in sensitized individuals has been derived from allergen-challenge models. To explore the dynamics of the cellular response during the actual disease, patients with a strictly seasonal allergic rhinitis were studied during natural allergen exposure. Ten patients suffering from an isolated birch-pollen allergy were followed from a symptom-free state before, during, and to the height of the birch-pollen season. Repeated parallel cell samplings from the nasal mucosa were performed with cytologic imprints on plastic strips, nasal lavages with the recovery of the cells in the lavage fluid with cytocentrifugation on object slides for cytologic study, and scrapings from the nasal surface with a curette for histologic and ultrastructural evaluation. The histamine content was determined in lavage fluid and cell pellets. The tosyl-alpha-tosyl-L-arginine methyl esterase activity of the nasal lavage fluid was also determined as a biochemical marker of the allergic inflammatory reaction. The birch-pollen season was moderate in terms of pollen counts, and this resulted in mild to moderate nasal symptoms that ran parallel to the birch-pollen counts. The total number of cells recovered in the lavage fluid was 1.2 +/- 0.4 (SEM) x 10(6) before and 3.2 +/- 2.0 per 10(6) cells (not significant) during pollen exposure. Most cells were neutrophils and mononuclear cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The cellular response of the human allergic mucosa to natural allergen exposure. 246 80

Basophils from five of six human donors released histamine in response to neutrophil attractant/activation protein-1 (NAP-1). Histamine release by this protein was concentration-dependent over the range of 3 x 10(-7) M to 4 x 10(-6) M. At 4 x 10(-6) M, the mean agonist-induced release was 16 +/- 3% (SEM) of total basophil histamine. For the same basophil preparations, release by anti-IgE was 35 +/- 6%. The chemotactic protein did not cause release of histamine from basophils at 0 degrees C or in the presence of 10 mM EDTA. The time-course of histamine release was rapid; release was 43% of maximal after 30 s and maximal after 1 min of incubation. Thus, in addition to its previously characterized neutrophil chemotactic and activating properties, this protein activates human basophils.
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PMID:Neutrophil attractant/activation protein-1 (NAP-1) causes human basophil histamine release. 247 83

In this study, we have explored the relationship between interleukins and human basophil activation. Previous studies by ourselves and others have found that recombinant human (rh) IL-3 causes histamine release. The ability to release histamine has also been claimed for IL-1 but we cannot confirm this. In experiments with the basophils of 29 donors (excluding one D2O responder), histamine release with 100 ng/ml rhIL-1 alpha was 1.3 +/- 1% (SEM), whereas with rhIL-1 beta, it was 0.8 +/- 1%. Both IL-1 alpha and -1 beta were also used at concentrations of 0.01 to 1000 ng/ml without causing release. Neither increasing the Ca2+ concentration nor adding D2O or cytochalasin B caused IL-1 alpha and -1 beta to become secretagogues. rhIL-1, however, did augment IgE-dependent histamine release. The enhancement was similar with both rhIL-1 alpha and -1 beta, i.e. they were dose-dependent between 0.1 and 3 ng/ml and reached a plateau from 3 to 100 ng/ml. At submaximal histamine release (less than 10%), there was enhancement of three IgE-dependent secretagogues: 125% with goat anti-human IgE (n = 7), 215% with Ag E (n = 10), and 260% with a histamine releasing factor (n = 7). Non-IgE-dependent stimuli (formyl-methionine-leucine-phenylalanine and the ionophore A23187, n = 10) were enhanced less than 5%. rhIL-1-enhancement persisted after cell washing (n = 10). rhIL-1 was active in preparations of 50 to 75% pure basophils in which mononuclear cells were reduced by greater than 95% (n = 4), and mAbH34 to IL-1 beta blocked the enhancement caused by that molecule. We postulate that basophils have an IL-1 receptor which, when occupied, upregulates the response to IgE-related signals. Thus, this work characterizes a second interaction between interleukins and the cells central to the allergic response.
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PMID:Recombinant human IL-1 alpha and -1 beta potentiate IgE-mediated histamine release from human basophils. 247 85

A sensitive gas chromatography-mass spectrometric method was used to measure the generation in whole blood of leukotriene B4 (LTB4), a potent stimulator of neutrophil chemotaxis, in eight patients with chronic granulocytic leukaemia (CGL) and 12 healthy controls. LTB4 was detectable in unstimulated samples from all the patients (mean 194 (70 SEM) pg/ml), and the capacity for LTB4 production after stimulation with calcium ionophore (A23187) was similar in patients (32.1 (11) ng/10(6) leucocytes) and controls (38.1 (4) ng/10(6) leucocytes). In response to stimuli which induce neutrophil activation, LTB4 production was significantly greater in the patients than in controls: 35.6 (13) v 13.0 (3) ng/ml, p less than 0.05 (f-met-leu-phe); and 42.4 (16) v 14.7 (4) ng/ml, p less than 0.02 (opsonised zymosan). Anti-IgE stimulated considerably more LTB4 production in patients with CGL than in controls (3.86 (1.6) v 0.83 (0.43) ng/ml; p less than 0.005) and this correlated significantly (p less than 0.05) with the basophil count. Neutrophil chemotaxis to LTB4, however, was significantly impaired in the patients with CGL even at the highest concentration of LTB4 (10(-5) M). Chemotaxis to f-met-leu-phe, phagocytosis, and bacterial killing were normal. Thus although LTB4 synthesis is normal or even enhanced in patients with CGL, specific defects in LTB4-mediated responses may contribute to neutrophil dysfunction in this disease.
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PMID:Leukotriene B4 synthesis and neutrophil chemotaxis in chronic granulocytic leukaemia. 285 Mar

Immunogold labeling and silver enhancement techniques are widely used to determine density and distribution of cell membrane receptors by light and transmission electron microscopy. However, these techniques have not been widely used for receptor detection by scanning electron microscopy. We used antigen- or protein A-conjugated colloidal gold particles, together with silver enhancement, sequential secondary and back-scattered electron imaging (SEI and BEI), and digital image processing, to explore cell surface distribution of IgE-receptor complexes on RBL-2H3 cells, a rat leukemia line that provides a model for the study of mucosal mast cells. Cells were first incubated with a monoclonal antidinitrophenol IgE (anti-DNP-IgE) that binds with high affinity to cell surface IgE receptors. The resulting IgE-receptor complexes were cross-linked either with the multivalent antigen, DNP-BSA-gold, or with a polyclonal anti-IgE antibody. Antibody-treated cells were labeled after fixation with protein A-gold. Fixed, gold-labeled cell monolayers were silver enhanced (or not), dehydrated, critical point-dried, and coated with gold-palladium (for SEI analysis) or carbon (for combined SEI/BEI analysis). They were observed in an Hitachi S800 SEM equipped with a field emission tip and a Robinson backscattered electron detector. An image processor (MegaVision 1024XM) digitized images directly from the S800 microscope at 500-1000 line resolution. Silver enhancement significantly improves detection of gold particles in both SEI and BEI modes of SEM. On gold-palladium-coated samples, 20-nm particles are resolved by SEI after enhancement. BEI resolves 15-nm particles without enhancement and 5- or 10-nm particles are resolved by BEI on silver-enhanced, carbon-coated samples. Neither BEI nor SEI alone can yield high resolution topographical maps of receptor distribution (BEI forms images on the basis of atomic number contrast which reveals gold but not surface features). Image analysis techniques were therefore introduced to digitize, enhance, and process BEI and SEI images of the same field of view. The resulting high-contrast, high-resolution images were superimposed, yielding well-resolved maps of the distribution of antigen-IgE-receptor complexes on the surface of RBL-2H3 mast cells. The maps are stored in digital form, as required for computer-based quantitative morphometric analyses. These techniques of silver enhancement, combined BEI/SEI imaging, and digital image analysis can be applied to analyze density and distribution of any gold-labeled ligand on its target cell.
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PMID:Mapping gold-labeled IgE receptors on mast cells by scanning electron microscopy: receptor distributions revealed by silver enhancement, backscattered electron imaging, and digital image analysis. 296 20

Sixteen patients with acne vulgaris were studied. All patients had severe inflammatory lesions, nodulocystic and conglobata. Of them, 12 was male and 4 female, their age was between 16 and 24 years old. In all the cases laboratory test to evaluate chemotactic, nitroblue-tetrazolium and lysosomal activity of granulocyte were performed. The protocol included in vitro incubations with and without autologous serum for considered their action on the phagocytic cell. The results shows an inhibitory action of the autologous serum in chemotactic (d-mean, 34.25%; SEM, 2.39, p less than 0.01), nitroblue-tetrazolium test (d-mean, 21.06%; SEM, 2.85, p less than 0.05), and lysosomal activity (d-mean, 21.43%; SEM, 2.80, p less than 0.05). The authors suggest that granulocyte alterations that occur in inflammatory forms of acne vulgaris is a secondary phenomenon may be caused by seric IgE or vasoactive substances released during immune responses.
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PMID:[Inhibition of the function of the neutrophil granulocyte caused by autologous serum from patients with acne vulgaris]. 297 40

Adenosine, when it is administered by inhalation to asthmatic subjects, is a potent bronchoconstrictor, although its mechanism of action is not known. Since adenosine has been demonstrated to potentiate IgE-dependent mediator release from mast cells, we have investigated the possible relationship between adenosine-induced bronchoconstriction and release of mast cell mediators in 14 asthmatic subjects. In the first study the effect of the putative mast cell-stabilizing drug cromolyn sodium (SCG) was observed on the dose-related changes in SGaw and FEV1 produced by inhaled adenosine and histamine in seven subjects. Inhaled SCG (20 mg) had no effect on the airway responses to histamine. In contrast SCG significantly protected against adenosine-induced bronchoconstriction in four of the seven subjects as reflected by a decrease in the airway response to the highest concentrations of adenosine, from 65 +/- 8% to 12 +/- 3% (mean +/- SEM) for SGaw and 31 +/- 7% to 8 +/- 3% for FEV1. Those three subjects whose adenosine response was unaffected by SCG had received regular SCG until 12 hr before the studies. In a separate study on eight subjects, a single inhalation of adenosine, causing a maximum 61 +/- 4% fall in SGaw at 10 min, had no significant effect on circulating levels of histamine, neutrophil chemotactic factor, or cyclic AMP. Together these two studies suggest that bronchoconstriction produced by adenosine is not a consequence of enhanced mast cell-mediator release and that the inhibitory effects of SCG occur by a mechanism other than through mast cell stabilization.
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PMID:Adenosine-induced bronchoconstriction in asthma: role of mast cell-mediator release. 298 12

Sympathomimetic agents are used to reverse the cardiovascular and respiratory abnormalities that are associated with anaphylactic shock. In addition, in vitro studies have demonstrated that beta-adrenergic stimulation modulates IgE-mediated release of chemical mediators. To separately evaluate the ability of isoproterenol, a beta-adrenergic agonist, to prevent mediator release and anaphylactic shock, as well as to reverse the cardiopulmonary manifestations of systemic anaphylaxis, we administered a continuous infusion of isoproterenol before and during canine anaphylactic shock. An intravenous injection of Ascaris suum antigen was used to produce shock, which was characterized by a 50 +/- 15% (mean +/- SEM) decrease in mean arterial blood pressure, a 30 +/- 8% decrease in cardiac output, and a 122 +/- 95% increase in total pulmonary resistance. These changes were associated with significant increases in plasma histamine concentrations from 1.1 +/- 0.1 to 158.4 +/- 137 ng/ml. Administration of a continuous infusion of isoproterenol during anaphylactic shock did not significantly improve any of these physiologic abnormalities. However, when isoproterenol was administered prior to the injection of antigen, these physiologic changes were prevented and histamine release was inhibited in a significant proportion of animals. In contrast, beta-adrenergic stimulation did not prevent nonimmunologic shock and mediator release induced with compound 48/80. We conclude that the administration of a beta-adrenergic agonist prevented the cardiopulmonary manifestations of anaphylactic shock by inhibiting mediator release and that the physiologic effects of isoproterenol administered during systemic anaphylaxis were minimal.
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PMID:Prevention of canine anaphylaxis with isoproterenol. 301 67

A method of isolation has been developed to purify mast cells from human lung tissue. The purification steps are: (1) dispersion of human lung tissue in single-cell suspensions by enzymatic digestion, (2) partial purification by counterflow centrifugal elutriation, (3) Percoll gradient centrifugation, and (4) enrichment of the mast cells by affinity chromatography using anti-human IgE-Sepharose. Enzymatic dispersion yielded 0.6 +/- 0.2 x 10(6) mast cells per gram wet tissue with purities of 3.3 +/- 1.0% (mean +/- SEM n = 3). Elutriation and gradient centrifugation yielded 0.36 +/- 0.05 x 10(6) mast cells per gram lung tissue in fractions with purities of 30.8 +/- 10.7%. Enriched mast cell fractions were combined, and disposed of contaminating cells by affinity chromatography, thereby yielding 0.25 +/- 0.03 x 10(6) mast cells per gram lung tissue, and improving the purity to 75.3 +/- 8.3%. The purified mast cells were intact and vitality exceeded 95%. In this way from 1 g wet lung tissue 0.25 +/- 0.03 x 10(6) mast cells may be isolated with a mean recovery of 41.7 +/- 2.4% and a mean purity of 75.3 +/- 8.3%.
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PMID:The isolation of human lung mast cells by affinity chromatography. 334 Aug 20

The metabolism of human IgE was studied in normals, severe atopics, and patients with the hyperimmunoglobulin E-recurrent infection (HIE; Job's) syndrome to determine whether IgE metabolism is altered in patients with marked elevation of serum IgE. Purified polyclonal 125I-IgE was administered intravenously and serial plasma and urine samples were obtained. After analysis, the metabolic data support previously published evidence that IgE (at concentrations found in normal individuals) is catabolized at a higher fractional rate than other immunoglobulins and is catabolized by both an intravascular and an extravascular pathway. In addition, the data show that the fractional catabolic rate for IgE is significantly less for the atopic patients (mean +/- SEM = 0.20 +/- 0.01) and for the HIE patients (0.15 +/- 0.02) than for the normal volunteers (0.52 +/- 0.06; P less than 0.01) and is inversely related (r = -0.851; P less than 0.001) to the serum IgE concentration. These findings have specific importance in showing that decreased fractional catabolic rate contributes substantially to elevation of IgE in atopic and HIE patients. In addition, the findings have general significance in that they lead to a unifying hypothesis of immunoglobulin catabolism.
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PMID:Metabolism of immunoglobulin E in patients with markedly elevated serum immunoglobulin E levels. 358 68


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