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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. To investigate the role of mast cells and eosinophils in the pathogenesis of nocturnal asthma, the plasma methylhistamine concentration, serum eosinophil cationic protein level and peak expiratory flow rate were measured 2-hourly for 24 h in 10 patients with nocturnal asthma and in 10 healthy control subjects. Nocturnal asthma was defined as at least one nocturnal awakening per week due to cough, wheeze or breathlessness with an average overnight fall in peak expiratory flow rate of at least 15% during a 2-week run-in period. 2. The lowest peak expiratory flow rate occurred at 02.00-04.00 hours in the group with nocturnal asthma, whose overnight fall in peak expiratory flow rate was 29 +/- 5% in comparison with 5 +/- 1% (means +/- SEM) in the normal subjects. 3. Plasma methylhistamine levels at night (0.200-04.00 hours) were lower than during the day (10.00-20.00 hours) in both asthmatic patients and normal subjects (asthmatic patients: day, median 0.22 ng/ml, 95% confidence intervals 0.18-0.34 ng/ml; night, 0.17 ng/ml, 0.13-0.24 ng/ml; P < 0.01; normal subjects: day, 0.31 ng/ml, 0.24-0.41 ng/ml; night, 0.24 ng/ml, 0.21-0.33 ng/ml; P < 0.01). 4. The serum eosinophil cationic protein level was higher by day (30 ng/ml, 8-47 ng/ml) than by night (21 ng/ml, 5-34 ng/ml; P < 0.04) in the group with nocturnal asthma, but did not change significantly with the time of day in the normal subjects (day: 8 ng/ml, 4-14 ng/ml; night: 8 ng/ml, 5-21 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Circulating histamine and eosinophil cationic protein levels in nocturnal asthma. 132 39

Eosinophils contain four principal cationic proteins, major basic protein (MBP), eosinophil-derived neurotoxin (EDN), eosinophil cationic protein (ECP), and eosinophil peroxidase (EPO). To determine the quantities of these proteins in granulocytes and whether they are specific to eosinophils, their concentrations in lysates of human granulocytes were measured using specific radioimmunoassays. The effect of different methods for eosinophil lysis on the recovery of the proteins was also studied. Maximal recovery occurred at pH 2 for MBP and pH 5.6 for the other granule proteins. The proteins cosedimented with eosinophils and their concentrations (mean +/- SEM) in ng/10(6) eosinophils (and in nM/10(6) eosinophils) were: MBP, 8,982 +/- 611 (641.6); EDN, 3,283 +/- 116 (178.4); ECP, 5,269 +/- 283 (250.9); and EPO, 12,174 +/- 859 (171.5). Basophils from a normal person contained (in ng/10(6) cells) MBP, 2,374; EDN, 214; ECP, 77; and EPO, 17. Highly purified neutrophils contained (in ng/10(6) cells) MBP, 3 +/- 0.5; EDN, 72 +/- 9; and ECP, 50 +/- 12. Therefore we conclude that these proteins are mainly expressed in eosinophils, but that certain ones are present in basophils and neutrophils.
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PMID:Eosinophil granule proteins in peripheral blood granulocytes. 146 33

The small intestines of healthy volunteers were challenged with ethanol during regional perfusion of a defined jejunal segment. Infusion of 30 mL of 5000 mmol/L ethanol to the perfused jejunal segment gave a maximum ethanol concentration of 973 +/- 98 (SEM) mmol/L in the jejunum lumen. This ethanol challenge induced within 20-30 minutes a 10-fold increase in albumin (P less than 0.001) and a two-fold increase in the glycosaminoglycan hyaluronic acid (P less than 0.05) in the perfusion fluid. Later during the challenge and simultaneously with a decreased jejunal loss of albumin, the jejunal recovery of prostaglandin E2 increased fourfold (P less than 0.01). The jejunal fluid concentrations of histamine and eosinophil cationic protein remained stable during the ethanol challenge. No changes in the jejunal appearance of albumin or other measured substances were seen when the maximum jejunal fluid concentrations of ethanol were less than 400 mmol/L achieved during challenge with smaller amounts of ethanol. The increased jejunal fluid appearance of hyaluronic acid after ethanol challenge indicates increased leakage from the interstitial/lymph fluid of the gut wall due to altered mucosal permeability. The relatively larger jejunal losses of albumin suggest that ethanol induces increased microvascular permeability of the jejunum as well.
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PMID:Acute exposure of small intestine to ethanol induces mucosal leakage and prostaglandin E2 synthesis. 173 17

To investigate the mechanisms of eosinophil activation in the airways of patients with asthma, we attempted to detect eosinophil-activating cytokines in sputum extracts obtained from asthmatic patients during acute attacks or in remission by eosinophil survival assay. Purified guinea pig eosinophils were cultured in the presence or absence of sputum extracts, and the eosinophil viability was measured on Day 4. Eosinophil viability in the presence of sputum extracts derived from patients during moderate or severe attacks was significantly higher than that for sputum obtained from patients in remission or during mild attacks or from those with other respiratory diseases, including bronchiectasis and diffuse panbronchiolitis (p < 0.05). The total symptom score during the week prior to sputum collection correlated with the eosinophil viability (rs = 0.79, p < 0.01). Eosinophil viability-enhancing activity (EVEA) in the sputum of asthmatic patients with moderate or severe attacks was neutralized by anti-IL-5 antibody and by anti-GM-CSF antibody by 19.9 +/- 13.7% and 76.9 +/- 8.2% (mean +/- SEM, n = 7), respectively. EVEA was completely neutralized by a combination of anti-IL-5 and anti-GM-CSF antibodies. There was a significant correlation between the concentration of eosinophil cationic protein (ECP) in sputum extracts and the eosinophil viability (rs = 0.54, p < 0.05). These findings suggest that IL-5 and GM-CSF are present in the sputum during asthma attacks and that these cytokines are at least partially responsible for eosinophil activation in asthma.
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PMID:Eosinophil viability-enhancing activity in sputum from patients with bronchial asthma, Contributions of interleukin-5 and granulocyte/macrophage colony-stimulating factor. 788 46

Eosinophil inflammation is essential in many cases of allergic and non-allergic rhinitis. Activated eosinophils release toxic granule proteins. In this study, we compared the degree of local nasal and systemic eosinophil activation by the determination of eosinophil cationic protein (ECP) in serum and native nasal fluid from 119 patients. We found no significant differences in serum ECP levels of the various patient groups. In all patient groups, except in the vasomotor rhinitis group, nasal fluid ECP levels differed significantly from normal controls. We found a nasal fluid ECP (mean +/- SEM) of 32.6 +/- 8.1 ng/ml for normals, 106 +/- 39.7 for non-rhinitic atopics, 87.6 +/- 20.8 ng/ml for patients with chronic non-allergic sinusitis, 101.3 +/- 40.4 ng/ml for patients with a history of pollinosis, 150.5 +/- 35.1 ng/ml for patients with acute pollinosis, 84.7 +/- 24.7 ng/ml for individuals with perennial allergic rhinitis and 112.9 +/- 25.6 ng/ml for patients with both perennial and seasonal allergy. Patients with nasal polyps had mean nasal ECP levels of 146.9 +/- 57.7 ng/ml in absence of allergy and 147.9 +/- 54.9 ng/ml in the presence of allergy. Nasal ECP was 67.0 +/- 22.4 for patients with hyperreactive rhinitis. We found a significant correlation of 0.95 between nasal eosinophils and nasal ECP. Nasal ECP and a subjective symptom score only correlate significantly for chronic sinusitis. We conclude that monitoring native nasal fluid ECP levels may be useful in the diagnosis and management of nasal inflammation. Elevated ECP in nasal secretion may originate from upregulated eosinophil degranulation and thus is a marker for local inflammation although not specific for any particular nasal disease.
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PMID:Eosinophil inflammation of the nasal mucosa in allergic and non-allergic rhinitis measured by eosinophil cationic protein levels in native nasal fluid and serum. 788 29

To determine whether induced sputum samples might provide a useful means for evaluating the effects of therapy on airway mucosal inflammation, we examined induced sputum samples obtained before and after 6 days of treatment with prednisone (0.5 mg/kg/day) or placebo in a randomized, double-blind study of 24 asthmatic subjects. Induced sputum was analyzed for total and differential cell counts and for concentrations of eosinophil cationic protein, albumin, and mucin-like glycoprotein. We found that the mean (+/- SEM) percentage of eosinophils in sputum samples from the prednisone-treated group fell from 14.1% +/- 5.0% at baseline to 1.8% +/- 0.8% after treatment, a decrease significantly greater than in the placebo-treated group (from 10.3% +/- 4.9% to 11.1% +/- 4.0%; p = 0.002). The absolute number of eosinophils also decreased significantly more in the prednisone-treated group than in the placebo-treated group (p = 0.04). In addition, eosinophil cationic protein levels in induced sputum fell more in the prednisone-treated group than in the placebo-treated group (from 324 +/- 131 ng/ml to 144 +/- 84 ng/ml vs 173 +/- 50 ng/ml to 188 +/- 47 ng/ml; p = 0.002). Furthermore, prednisone treatment was associated with a significant increase in peak expiratory flow, an effect that was significantly correlated with the decrease in eosinophil percentage in induced sputum (rs = 0.64, p = 0.04). Prednisone treatment was not associated with any significant change in the concentrations of albumin or mucin-like glycoprotein. We conclude that analysis of induced sputum is a useful noninvasive method for studying the effects of asthma therapy on airway eosinophilic inflammation.
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PMID:Analysis of induced sputum to examine the effects of prednisone on airway inflammation in asthmatic subjects. 796 55

To determine the feasibility of cellular and biochemical analysis of sputum induced after inhalation of hypertonic (3%) saline, we analyzed sputum induced in 10 healthy and in 18 asthmatic subjects. We also analyzed saliva samples from all subjects. The entire sputum sample and the saliva sample were reduced using dithiothreitol, and cell counts and differentials were determined. Biochemical analysis was performed on sputum and saliva supernatants obtained after centrifugation. We found that induced sputum from asthmatic subjects had a higher percentage of eosinophils [8.1 +/- 3.43 (mean +/- SEM) versus 0.03 +/- 0.02%, p < 0.009] (after excluding squamous cells) and also had higher levels of albumin (232.3 +/- 54.8 versus 79.5 +/- 9.7 micrograms/ml, p < 0.02), fibrinogen (44.2 +/- 11.6 versus 11.9 +/- 2.5 micrograms/ml, p < 0.008) and eosinophil cationic protein (ECP) (142.6 +/- 34.2 versus 26.1 +/- 4.7 ng/ml, p < 0.006) but not of histamine or tryptase. In saliva, squamous cells made up more than 99% of the cells in both groups, and protein concentrations were not significantly different. We conclude that cellular and biochemical analysis of induced sputum is feasible in healthy and in asthmatic subjects and that it reveals differences similar to those reported from analyses of bronchial lavage fluid.
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PMID:Cellular and biochemical analysis of induced sputum from asthmatic and from healthy subjects. 848 20

Eosinophils (Eo) play a significant role in allergic inflammation and the host's immunity to parasitic infections. Although the presence of C1q-binding cell surface molecule(s) (C1q-R) on Eo had been previously implicated by the ability of C1q to augment IgG-dependent, Eo-mediated killing of schistosomula, little is known about the structure or the function of this receptor. The present studies were therefore undertaken to immunochemically demonstrate and to examine the biology of Eo C1q-R. Eo were purified to homogeneity (>90%) and viability (>98%) from hypereosinophilic donors by Percoll density gradient. Western blot analysis using antibodies to cC1q-R and gC1q-R showed distinct bands corresponding to cC1q-R (60 kDa) and gC1q-R (33 kDa) when immunoblotted with their respective antibodies. The Eo C1q-R was tested for its ability to induce chemokinesis and/or chemotaxis as assessed by the modified Boyden microchamber assay utilizing 5-micrometer-pore polycarbonate membranes and using C1q, cC1q, or gC1q (10 micrograms/ml) as agonists. The known chemotactic factors C5a and RANTES (10(-8)M) were used as positive controls. The results showed that at this concentration, cC1q was most efficient in its ability to induce Eo migration (20 +/- SEM 12, n = 4) followed by C1q (107 +/- SEM 7, n=7) and gC1q (77 +/- SEM 10, n = 10). When checkerboard analysis was performed, the data indicated that the observed phenomenon was likely to be due largely to chemokinesis. As expected, C5a (145 +/- SEM 15, n = 7) and RANTES (145 +/- SEM 43, n = 7) were both chemotactic. Furthermore, incubation of Eo with 50 micrograms of either C1q, gC1q, or cC1q (1 hr, 37 degrees C) did not cause release of eosinophil cationic protein as measured by RIA, nor did it enhance the expression of CD11b or CD29 as assessed by FACS analysis. The data presented in this paper show that Eo express both cC1q-R and gC1q-R and may participate in Eo function by providing a primary signal for locomotion.
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PMID:Human C1q induces eosinophil migration. 880 41

Here we show that the supernatant from activated lung mast cells induced the release of eosinophil cationic protein (ECP) from eosinophils. Lung mast cells were purified using affinity magnetic selection with monoclonal antibody (mAb) YB5.B8 to achieve a final mast cell purity of 93-99%. Eosinophils were purified by immunomagnetic negative selection (>98.0% pure). The supernatant was obtained from lung mast cells activated for 24 h with 1 microg/ml anti-IgE and 50 ng/ml stem cell factor (SCF). Human eosinophils were incubated with various concentrations of the supernatants for 4 h and ECP released was measured by RIA. Using 4 different donors' supernatant from mast cells, each donor's supernatant caused a dose-dependent release of ECP from eosinophils. The dilutant of 1:2 (v/v) of the supernatant induced 657.5 +/- 55.6 ng/10(6) eosinophils of ECP which is statistically significant (p = 0.008, n = 4) compared with the culture medium alone. Anti-interleukin (IL-5 neutralizing mAb, 10 microg/ml, and anti-tumor necrosis factor-alpha (TNF alpha) neutralizing mAb, 10 microg/ml, significantly inhibited the supernatant-induced ECP release in 79.3 +/- 9.4 and 68.2 +/- 14.1% (mean +/- SEM, n = 6, p < 0.005), respectively. Anti-granulocyte/macrophage colony-stimulating factor (GM-CSF) neutralizing mAb, 50 microg/ml, caused 68.0 +/- 6.1% of inhibition (p = 0.002). The isotype negative control had no measurable inhibitory or stimulatory effect for the stimuli. We confirmed that mast cells produce IL-5, GM-CSF and TNF alpha in response to IgE-dependent stimulation by using RT-PCR, in situ hybridization, ELISA and immunocytochemistry. A million of lung mast cells generated 41.4 pg (7.0-273.6) (median with range) of TNF alpha, 252.6 pg (158.7-3,652) of GM-CSF and 735 pg (< 10-2,750) of IL-5 24 h after activation with SCF and anti-IgE. These findings indicate that the human mast cells may contribute to the chronicity of tissue inflammation.
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PMID:Activation of eosinophils with cytokines produced by lung mast cells. 936 32

The hypotheses tested in this study were that during acute asthma exacerbations (1) exhaled nitric oxide concentrations [eNO] are a more sensitive, noninvasive indicator of asthma disease activity than serum markers of inflammation such as eosinophil cationic protein (ECP) or soluble interleukin 2 receptor (sIL2R), and (2) elevated [eNO] are reduced after treatment with glucocorticoids (GC). Peak eNO levels were measured by chemiluminescence during slow expiration. Seven asthmatic subjects (mean age 11 yrs; mean morning FEV1 65% predicted) receiving inhaled GC, and with no radiographic evidence of acute sinusitis, were studied before and after a course of oral GC. Measurements of [eNO], ECP and sIL2R levels, and FEV1% were obtained before and after a course of GC. Six atopic nonasthmatic subjects (mean age 12 years; mean FEV1 94% predicted) and seven normal subjects (mean age 13 years; mean FEV1 100% predicted) were studied. The mean peak [eNO] level (parts per billion: ppb) for the asthma subjects before treatment (52 +/- 5 ppb SEM) was greater than the value for both nonasthmatic atopic and normal subjects (16 +/- 2 ppb and 14 +/- 2 ppb SEM, respectively; P < 0.0001). There was no significant difference in ECP or sIL2R values between asthmatic subjects and either atopic or normal subjects (P > 0.05). Baseline pre-GC treatment ECP levels in the asthmatic subjects were significantly higher (P < 0.002) than post-GC treatment values. The mean peak [eNO] level in the asthmatic subjects declined after oral GC treatment to 14 +/- 1 ppb (P < 0.0002) and was less than 2 ppb different from either control group (P > 0.75). We conclude that [eNO] is a more sensitive marker of asthma disease activity than ECP and sIL2R levels. In addition, [eNO] appears to be a more useful indicator of the beneficial response to GC therapy than these other measurements in pediatric asthma.
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PMID:Comparison of exhaled nitric oxide, serum eosinophilic cationic protein, and soluble interleukin-2 receptor in exacerbations of pediatric asthma. 940 62


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