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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
    Nasal and bronchial response to exercise in patients with asthma and rhinitis: the role of nitric oxide (2005)
    Oxford, UK : Munksgaard International Publishers
    Allergy 60 (2005), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background:  Physical exercise is associated with a decrease in nasal resistance in rhinitis and an increase in bronchial resistance in asthma. The objective was to evaluate the relationship between the levels of nasal nitric oxide (nNO) and exhaled bronchial nitric oxide (eNO) with bronchial responses to exercise in patients with rhinitis and asthma.Methods:  We submitted 24 subjects with asthma and rhinitis to an exercise test. A decrease in FEV1≥15% was considered positive. The volume of the nasal cavity and the minimal cross-sectional area (MCA) was evaluated by means of acoustic rhinometry (AR), and nNO and eNO were evaluated by chemoluminiscence. The measurements were recorded at baseline, 15 and 50 min after the end of the exercise test.Results:  The exercise test was positive in 17 cases. Fifteen minutes after exercise test, the nasal volume increased by 57% (P 〈 0.0001) and was still increased by 30% after 50 min (P 〈 0.0001). There was no correlation between decrease in FEV1 and increase in nasal volume. The baseline value of nNO was 1185 ± 439 ppb, and the value at 15 and 50 min was 1165 ± 413 and 1020 ± 368 ppb, the latter value being significantly lower (P 〈 0.01) than the baseline. The baseline value of eNO was 21 ± 19 ppb, with no significant differences at 15 and 50 min. There was no significant correlation between either the decrease in FEV1 and the nasal response, or the baseline eNO and nNO values.Conclusions:  The nasal and bronchial response to exercise is completely different in rhinitis and asthma; in the former, an increase in nasal volume occurs, while in the latter there is a drop in FEV1. There is no relationship between the values of nasal or exhaled NO and the nasal and bronchial response after exercise.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1398-9995.2005.00835.x
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  • 3
    Electronic Resource
    Electronic Resource
    Glucocorticoid receptors in human airways (2004)
    Oxford, UK : Munksgaard International Publishers
    Allergy 59 (2004), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Inhaled and intranasal glucocorticoids are the most common and effective drugs for controlling symptoms and airway inflammation in respiratory diseases such as asthma, allergic rhinitis, and nasal polyposis. The last few years have seen a growing understanding of the mechanisms of glucocorticoid action and, in particular, the receptor that mediates glucocorticoid actions, the glucocorticoid receptor (GR). In this revision we present an update on the GR gene, the expression and regulation of its gene products, namely GRα and GRβ, as well as their alterations in pathological states. GRα is responsible for the induction and repression of target genes, it is expressed in virtually all human cells and tissues, and its expression is known to be downregulated by glucocorticoids. GRβ has been found to act as a dominant negative inhibitor of GRα-mediated transactivation in in vitro studies with transfected cells, but it does not appear to have a significant inhibitory effect on GRα-mediated transrepression. In addition, for most tissues the expression of GRβ, at least at the mRNA level, is extremely low compared with that of GRα. Some pro-inflammatory cytokines appear to upregulate the expression of GRβ, and increased GRβ expression has been reported in diseases associated with glucocorticoid resistance or insensitivity, such as bronchial asthma, nasal polyposis, and ulcerative colitis. However, the possible role of GRβ in modulating glucocorticoid sensitivity and/or resistance in vivo has been highly debated and it is not yet clear.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1398-9995.2004.00635.x
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  • 4
    Electronic Resource
    Electronic Resource
    Nuclear factor-κB activity is down-regulated in nasal polyps from aspirin-sensitive asthmatics (2003)
    Oxford, UK : Munksgaard International Publishers
    Allergy 58 (2003), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: We examined whether a decreased activity of nuclear factor(NF)-κB), a transcriptional regulator of cyclooxygenase-2 (COX-2), could account for down-regulation of COX-2 in nasal polyps of aspirin-sensitive asthmatics.Methods: Nasal polyps were obtained from 17 aspirin-intolerant asthma/rhinitis patients (AIAR; 7 men, mean age 48 ± 12 years) and 23 aspirin-tolerant asthma/rhinitis patients (ATAR; 12 men, mean age 65 ± 11 years). COX-2 mRNA expression was measured using semiquantitative reverse transcriptase competitive polymerase chain reaction (RT-PCR), and the results were expressed as mean ± standard error of 106 molecules of mRNA/µg of total RNA. NF-κB binding was measured with 32P-labeled oligonucleotides and electrophoretic mobility shift assay (EMSA), and the results were expressed as a percentage with respect to the mean EMSA obtained in 19 healthy nasal mucosa.Results: The mean levels of COX-2 mRNA expression (0.25 ± 0.06) and NF-κB activity (89 ± 13) in nasal polyps from AIAR were significantly lower than in polyps from ATAR (COX-2 = 1.58 ± 0.50, and NF-κB = 143 ± 12, P 〈 0.01 and P 〈 0.05, respectively). Levels of COX-2 mRNA and NF-κB activity in polyps from patients on corticosteroid therapy did not differ statistically from those who were not on this therapy before polypectomy.Conclusion: This study shows that the low expression of COX-2 mRNA in nasal polyps from aspirin-sensitive patients is associated with a down-regulation of NF-κB activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1398-9995.2003.23792.x
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  • 5
    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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  • 6
    Electronic Resource
    Electronic Resource
    Early and late-phase asthmatic reactions: a hypothesis (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Allergy 47 (1992), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Why might a foreign particle, exercise or fog inhalation precipitate two asthmatic reactions? It is reasonable to suspect that asthmatic patients develop two reactions because healthy subjects may also develop two physiological responses to the same stimuli. This suggestion is supported by the observation that living things have developed adaptative systems to confront either sudden or persistent changes in the environment or within the internal milieu. The results of several studies suggest that the early phase response (EPR) usually involves cells which are normal residents of the respiratory epithelium (mast cells) and pre-formed substances (histamine), whereas cells participating in the late phase reaction (LPR) are recruited from the circulation (eosinophils, basophils and T cells). Up to now most of the studies of the EPR and LPR have been addressed to detecting a cell or metabolite abnormality. This simplistic approach would probably not improve the knowledge of the mechanisms involved in asthmatic responses. Since the presence of isolated or dual responses seems to depend on the intensity and duration of the stimuli it is reasonable to suspect that EPR and LPR are the result of an excessive adaptative response of the bodies of asthmatics to sudden and prolonged/strong stimuli, respectively.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1398-9995.1992.tb02064.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
    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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