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  • 1
    Electronic Resource
    Electronic Resource
    Regulation of ICAM-3 and other adhesion molecule expressions on eosinophils
in vitro. Effects of dexamethasone (1999)
    Copenhagen : Munksgaard International Publishers
    Allergy 54 (1999), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: ICAM-3 has been recently identified as the third leukocyte-function associated-1 (LFA-1) ligand. ICAM-3 is expressed in eosinophils, but its regulation has not been studied. The objective of this study was to investigate the differential expression of ICAM-3 and other adhesion molecules (AM) on the surface of eosinophils. We also evaluated the effects of dexamethasone on AM expression. Methods: Normodense eosinophils were isolated from peripheral blood and incubated with calcium ionophore A23187 (calcimycin) with and without dexamethasone. Expression of AM was assessed by flow cytometry and expressed as fluorescence mean intensity (FMI). Results: Peripheral blood eosinophils constitutively expressed low levels of ICAM-1 and ICAM-2 (〈10 FMI), moderate levels (10–50 FMI) of CD29 and L-selectin, and high levels (〉50 FMI) of ICAM-3, LFA-1, and Mac-1. Calcium ionophore (1 μM) significantly increased Mac-1 and ICAM-1 expression at 6 and 24 h. L-selectin expression decreased at 6 and 24 h, but ICAM-2, ICAM-3, LFA-1, and CD29 expression did not show any significant change after calcium ionophore stimulation. Dexamethasone decreased ICAM-3 and increased L-selectin basal expression, and it caused a dose-related inhibition of calcium ionophore-induced ICAM-1 expression. Conclusions: These findings suggest that some AM, such as ICAM-1, Mac-1, and L-selectin, may be involved in adhesion during eosinophil activation and that glucocorticoids may prevent airway inflammation by regulating the expression of AM in eosinophils. The role of ICAM-3, a leukocyte AM highly expressed in resting eosinophils, remains to be clarified.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1398-9995.1999.00251.x
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  • 2
    Electronic Resource
    Electronic Resource
    Aspirin-intolerant asthma: role of cyclo-oxygenase enzymes (2002)
    Oxford, UK : Blackwell Science, Ltd
    Allergy 57 (2002), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Aspirin-induced asthma and rhinitis (AIAR) appear to be precipitated by the inhibition of cyclo-oxygenase (COX). By inhibiting COX pathway aspirin diverts arachidonic acid metabolites to the lipoxygenase pathway. There are two isoforms of COX, namely COX-1 and COX-2. Metabolites derived from COX-1 are involved in cellular housekeeping functions. COX-2 can be induced in cells exposed to proinflammatory substances and growth factors. Recent studies have reported that patients with AIAR have decreased activity of COX-2 and lower production of PGE2 in the upper airway and peripheral blood cells. Considering the protective effect of exogenous PGE2 on aspirin-induced bronchoconstriction and the interdependence of PGE2 and cisteinyl leukotriene production, a reduced PGE2 synthesis may render aspirin-sensitive patients more susceptible to the inhibitory effect of NSAIDs drugs and also lead to an increase in cysteinyl leukotriene release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1398-9995.57.s72.14.x
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  • 3
    Electronic Resource
    Electronic Resource
    Oral and inhalation provocation tests for the diagnosis of
aspirin-induced asthma (2001)
    Copenhagen : Munksgaard International Publishers
    Allergy 56 (2001), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1398-9995.2001.00025.x
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  • 4
    Electronic Resource
    Electronic Resource
    NSAID-sensitive patients tolerate rofecoxib (2002)
    Oxford, UK : Munksgaard International Publishers
    Allergy 57 (2002), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1398-9995.2002.23893_6.x
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  • 5
    Electronic Resource
    Electronic Resource
    Non-steroidal anti-inflammatory drugs-induced urticaria and angioedema: more research on mechanisms needed (2005)
    Oxford, UK : Blackwell Publishing
    Clinical & experimental allergy 35 (2005), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.2005.02276.x
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  • 6
    Electronic Resource
    Electronic Resource
    Effects of topical anti-inflammatory drugs on eosinophil survival primed by epithelial cells. Additive effect of glucocorticoids and nedocromil sodium (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 27 (1997), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Eosinophil infiltration is a hallmark of the inflammatory response in rhinitis and in nasal polypcsis.Objective We studied the effect of steroids and nedocromil sodium on eosinophil survival primed by epithelial cells from healthy (nasal mucosa) and inflamed (nasal polyp) respiratory tissue.Methods Blood eosinophils were incubated with increasing concentrations (10-11 10-5 M) of topical steroids (fiuticasone propionate, budesonide, triamcinolone acetonide and beclomethasone dipropionate) and/or nedocromil sodium prior to the addition of human epithelial cell conditioned media (HECM), eosinophil viability was measured and IC50 for each drug was calculated.Results All four steroids and nedocromil sodium caused a dose-related inhibition of HECM-induced eosinophil survival. The IC50 of steroids were lower in eosinophils primed by mucosa HECM than on those primed by polyp HECM (fluticasone, 4nM vs 114nM: budesonide, 21 nM vs 280 nM; triamcinolone, 7 nM vs 853 nM; and beclomethasone, 171 nM vs 181 nM). The combined inhibitory effect of 10-7M budesonide plus 10-5M nedocromil (43.8 ± 10.8%, P 〈 0.03) was significantly higher than budesonide (28.5 ± 9.2%) or nedocromil (16.7 ± 5.4%) alone and close to 10-5M budesonide (52.3 ± 11%). No differences were found in cytokine (IL-8, IL-6, GM-CSF, TNFα, IL-lβ and RANTES) concentrations between HECM from mucosa and polyps.Conclusion These results suggest that topical anti-inflammatory drugs may diminish airway eosinophilic infiltration by decreasing eosinophil viability, that nasal polyp epithelial cell secretions may induce steroid resistance in eosinophils, and that nedocromil sodium has additive effects with steroids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2222.1997.1750975.x
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  • 7
    Electronic Resource
    Electronic Resource
    Cytokine gene expression and release from epithelial cells. A comparison study between healthy nasal mucosa and nasal polyps (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 25 (1995), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Backgroud Epithelial cells release cytokines and they probably contribute to chronic inflammation detected in bronchial asthma, rhinitis and nasal polyposis.Objectives To investigate the effect of cultures on cytokine gene expression to compare epithelial cell cytokine release by both healthy nasal nucosa (HNM) and nasal polyps (NP), and the modulation by dexamethasone and to investigate which cytokines may promote eosinophil survival.Methods Epithelials cells were cultured to confluence, human epithelial cell conditioned media generated with or without dexamethasone, and supernalanls measured by ELISA. Cytokine gene expression was investigated by reverse transcription-polymerase chain reaction (RT-PCR).Results Fresh epithelial cells only expressed mRNA for intesleukin-8 (IL-8) and granulocyte macrophage-colony stimulating factor (GM-CSF) while cultured cells expressed mRNA for IL-1β IL-6, IL-8, tumour necrosis factor-α (TNFα) and GM-CSF. Epithelial cells from NP significantly (P 〈 0.05) released more IL-8 (25431 ± 3163 pg/mL), and GM-CSF (1229 ± 391 pg/mL) than those from HNM (18604 ± 1723pg/mL for IL-8; and 611 ± 98 pg/mL for GM-CSF), Dexamethasone 10 μM inhibited the release of all cytokines, this effect being similar (40 50%) in both HNM and NP. except for IL-6 which was higher in HNM. Eosinophil survival induced by epithelial cell secretions from both HNM and NP was strongly blocked by GM-CSF antibody while it was partially blocked by antibodies to TNFα and IL-8.Conclusions These findings suggest that although epithelial cell culture procedures may upregulate cytokine gene expression, nasal polyps may represent a more active inflammatory tissue by releasing more cytokines than healthy nasal mucosa this release being inhibited by steroids; and that, in addition to GM-CSF.other cytokines such as TNFo and IL-8, may also be involved in the promotion of eosinophil survival.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.1995.tb01108.x
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  • 8
    Electronic Resource
    Electronic Resource
    Comparison of the role of nasal polyp and normal nasal mucosal epithelial cells on in vitro eosinophil survival. Mediation by GM–CSF and inhibition by dexamethasone (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 24 (1994), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Eosinophilic infiltration of the respiratory mucosa is considered an inflammatory hallmark of allergic rhinitis, bronchial asthma and nasal polyposis. However, the mechanisms involved in this infiltration have not yet been totally elucidated. The objective of this study was to investigate and compare the influence of epithelial cell secretions from both nasal polyps (NP) and normal nasal mucosa (NM) on in vitro eosinophil survival. Epithelial cells were identified by microscopy; and immunohislochemisiry. cultured to confluence, and human epithelial cell conditioned media (HECM) was generated from cultures. Eosinophits were isolated at high viability and purity (〉90%) from peripheral blood and incubated with HECM. HECM from both NM and NP increased eosinophil survival in a dose-dependent manner, this effect being maximal at a concentration of 25% for NM (73.4%±5.5%, n= 26, P〈 0.001) and of 10% for NP (74.5%± 84%n= 18, P 〈 0.001). Incubation of monoclonal antibody to human GM-CSF with HECM, neutralized the induction of eosinophil survival by HECM from both NM and NP. HECM from NP contained higher concentrations of GM-CSF (111 ± 25.4 pg/ml, n= 17) than HECM from NM (97.1 ± 15.2 pg/ml. n= 8). without reaching statistical significance. Pre-incubation of dexamethasone with eosinophils also blocked HFCM-induced eosinophil survival from both NM (10−8-10−5 M; IC50 = 9.5 nM) and NP (10-7-10-5 M; IC50 = 83 nM). These results suggest that: firstly eosinophil infiltration into the respiratory mucosa during allergic reaction and nasal polyposis may be modulated at least in part by GM-CSF from epithelial cells; and secondly epithelial cells from NP might have a more potent effect on inducing eosinophil infiltration of the respiratory mucosa than epithelial cells from NM. Finally, we may consider this as a reliable in vitro model to compare the role of epithelial cells from inflammatory (NP) and non-inflammatory (NM) tissue in respiratory inflammation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.1994.tb00240.x
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  • 9
    Electronic Resource
    Electronic Resource
    Response of nose and bronchi to exercise in asthma and rhinitis: similarities and differences (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 26 (1996), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The response of asthmatic patients to exercise differs from that of healthy subjects, and the mechanisms responsible for the exercise-induced bronchoconstriction in the former group remain uncertain. The severity of bronchospasm may be related to water loss from the respiratory tree, but there are conflicting explanations for this.The response of the nose to exercise, in healthy subjects or in patients with asthma and rhinitis, has been the subject of few investigations, but a recent study found that the nose responds in a different fashion to the bronchi in patients with rhinitis and asthma. The bronchial tree responds by narrowing, while the nose becomes more patent. There is evidence that the bronchi are the main sites of airway narrowing in exercise-induced bronchoconstriction, while there can also be simultaneous tracheal dilatation. In addition, it now appears that the nasal response to exercise in all subjects parallels that of the trachea. In total, the results suggest that different mechanisms are responsible for regulating the patency of the upper and lower airways.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.1996.tb00657.x
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  • 10
    Electronic Resource
    Electronic Resource
    COX-1 sparing drugs in aspirin-sensitive asthma (2001)
    Oxford, UK : Blackwell Science, Ltd
    Clinical & experimental allergy 31 (2001), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2222.2001.01101.x
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