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See detailDisturbed Cytokine Production at the Systemic Level in Difficult-to-Control Atopic Asthma: Evidence for Raised Interleukin-4 and Decreased Interferon-gamma Release following Lipopolysaccharide Stimulation.
MANISE, Maïté ULg; SCHLEICH, FLorence ULg; QUAEDVLIEG, Valérie ULg et al

in International Archives of Allergy & Immunology (2012), 158(1), 1-8

Background: Disturbed cytokine production is thought to govern inflammation in asthma, which, in its turn, may lead to uncontrolled disease. The aim of this study was to assess the relationship between ... [more ▼]

Background: Disturbed cytokine production is thought to govern inflammation in asthma, which, in its turn, may lead to uncontrolled disease. The aim of this study was to assess the relationship between cytokine production from blood leucocytes and the level of asthma control. Methods: We compared the production of interleukin (IL)-4, IL-6, IL-10, interferon (IFN)-gamma and tumour necrosis factor-alpha from peripheral blood leucocytes in non-atopic healthy subjects (n = 22), atopic non-asthmatics (n = 10), well-controlled asthmatics [Juniper asthma control questionnaire (ACQ) score <1.5; n = 20] and patients with uncontrolled asthma despite inhaled or oral corticoids (ACQ score >/=1.5; n = 20). Fifty microlitres of peripheral blood was incubated for 24 h with RPMIc, lipopolysaccharide (LPS; 1 ng/ml) or phytohaemagglutinin (1 mug/ml), and cytokines were measured by immunotrapping (ELISA). Results: Both controlled and uncontrolled asthmatics as well as atopic non-asthmatics spontaneously produced more IL-4 than non-atopic healthy subjects (p < 0.001). IL-4 production induced by LPS was significantly greater (p < 0.05) in both asthma groups compared to atopic non-asthmatics and non-atopic healthy subjects. By contrast, IFN-gamma release induced by LPS was lower in uncontrolled asthmatics than in non-atopic healthy subjects (p < 0.05) and controlled asthmatics (p < 0.05). IL-10 release after LPS was greater in uncontrolled asthmatics than in atopic non-asthmatics (p < 0.05). No difference was observed regarding other cytokines. Conclusion: Blood cells from patients with difficult-to-control atopic asthma display highly skewed Th2 cytokine release following LPS stimulation. [less ▲]

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See detailComparison of acute inflammatory and chronic structural asthma-like responses between C57BL/6 and BALB/c mice
Van Hove, C. L.; Maes, T.; Cataldo, Didier ULg et al

in International Archives of Allergy & Immunology (2009), 149(3), 195-207

BACKGROUND: The interactions between airway responsiveness, structural remodelling and inflammation in allergic asthma remain poorly understood. Prolonged challenge with inhaled allergen is necessary to ... [more ▼]

BACKGROUND: The interactions between airway responsiveness, structural remodelling and inflammation in allergic asthma remain poorly understood. Prolonged challenge with inhaled allergen is necessary to replicate many of the features of airway wall remodelling in mice. In both mice and humans, genetic differences can have a profound influence on allergy, inflammation, airway responsiveness and structural changes. METHODS: The aim of this study was to provide a comparative analysis of allergen-induced airway changes in sensitized BALB/c and C57BL/6 mice that were exposed to inhaled allergen for 2 ('acute'), 6 or 9 weeks ('chronic'). Inflammation, remodelling and responsiveness were analyzed. RESULTS: Both strains developed a Th-2-driven airway inflammation with allergen-specific IgE, airway eosinophilia and goblet cell hyperplasia upon 2 weeks of allergen inhalation. This was accompanied by a significant increase in airway smooth muscle mass and hyperresponsiveness in BALB/c but not in C57BL/6 mice. However, airway eosinophilia was more pronounced in the C57BL/6 strain. Chronic allergen exposure (6 or 9 weeks) resulted in an increase in airway smooth muscle mass as well as subepithelial collagen and fibronectin deposition in both strains. The emergence of these structural changes paralleled the disappearance of inflammation in both C57BL/6 and BALB/c mice and loss of hyperresponsiveness in the BALB/c strain. TGF-beta(1 )was accordingly elevated in both strains. CONCLUSION: Airway inflammation, remodelling and hyperresponsiveness are closely intertwined processes. Genetic background influences several aspects of the acute allergic phenotype. Chronic allergen exposure induces a marked airway remodelling that parallels a decreased inflammation, which was largely comparable between the two strains. [less ▲]

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See detailMatrix metalloproteinase-12 and cathepsin D expression in pulmonary macrophages and dendritic cells of cigarette smoke-exposed mice
Bracke, K.; Cataldo, Didier ULg; Maes, T. et al

in International Archives of Allergy & Immunology (2005), 138(2), 169-179

An imbalance between proteinases and their inhibitors is believed to play an essential role in the development of chronic obstructive pulmonary disease ( COPD) and pulmonary emphysema. COPD is mainly ... [more ▼]

An imbalance between proteinases and their inhibitors is believed to play an essential role in the development of chronic obstructive pulmonary disease ( COPD) and pulmonary emphysema. COPD is mainly caused by cigarette smoking, and is characterized by an increase in inflammatory cells in small airways and lung parenchyma. We examined the mRNA expression of several proteinases in lungs of mice exposed to cigarette smoke or control air. After 1, 3 and 6 months' smoke exposure there was a significant increase of matrix metalloproteinase (MMP)-12 and Cathepsin D mRNA, compared to air-exposed mice. To determine the cellular origin of MMP-12 and Cathepsin D, we isolated dendritic cells (DCs) and macrophages from the lungs of mice. There was an increase in MMP-12 mRNA after smoke exposure in both macrophage and DC populations, whereas Cathepsin D was predominantly expressed in macrophages. Immunohistochemistry clearly revealed the expression of Cathepsin D protein in alveolar macrophages of cigarette smoke-exposed mice, in contrast to air-exposed littermates. Western blots on lung tissue demonstrated an increase of MMP-12 protein in cigarette smoke- exposed animals. These results indicate that cigarette smoke increases the expression of MMP-12 and Cathepsin D in the lungs of mice, and that not only macrophages but also DCs produce MMP-12. Copyright (C) 2005 S. Karger AG, Basel. [less ▲]

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See detailNovel treatments for drug-induced toxic epidermal necrolysis (Lyell's syndrome).
Paquet, Philippe ULg; Pierard, Gérald ULg; Quatresooz, Pascale ULg

in International Archives of Allergy & Immunology (2005), 136(3), 205-16

Drug-induced toxic epidermal necrolysis (TEN) is a life-threatening disease characterized by extensive destruction of the epidermis. It apparently results from the formation of specific toxic drug ... [more ▼]

Drug-induced toxic epidermal necrolysis (TEN) is a life-threatening disease characterized by extensive destruction of the epidermis. It apparently results from the formation of specific toxic drug metabolites by the keratinocytes. The mortality rate which averages 25-30% is mainly due to secondary septicemia, and to ionic and metabolic disturbances following loss of epidermal integrity. Apoptosis is the likely mechanism leading to massive keratinocyte death in TEN. Dysregulations in the tumor necrosis factor-alpha (TNF-alpha) pathway, CD95 system (Fas ligand, CD95L; Fas receptor, CD95R) and calcium homeostasis in the epidermis are involved in this apoptotic process. An active role has also been ascribed to T lymphocytes, macrophages and factor XIIIa-positive dermal dendrocytes. Despite progress, treatment of TEN remains controversial. In the past, systemic glucocorticoids were used in order to target the inflammatory reaction in TEN. However, there was no evidence for improvement of the healing process, while corticosteroids worsened the prognosis by increasing the risk of septicemia. Only a few cases have been treated with other drugs including cyclophosphamide, pentoxyfilline, thalidomide, anti-TNF-alpha antibodies and cyclosporin A. In the recent past, some TEN patients were treated with intravenous human immunoglobulins (IVIG). The rationale for such a treatment was to block the CD95 system on keratinocytes. The early promising clinical results of IVIG treatment in TEN were subsequently challenged. This review compares the effectiveness and drawbacks of the major drugs presently used in TEN treatment. Some future prospects in TEN management are also discussed. [less ▲]

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See detailMMP-2 and MMP-9-Linked Gelatinolytic Activity in the Sputum from Patients with Asthma and Chronic Obstructive Pulmonary Disease
Cataldo, Didier ULg; Munaut, Carine ULg; Noël, Agnès ULg et al

in International Archives of Allergy & Immunology (2000), 123(3), 259-67

BACKGROUND: The course of asthma and chronic obstructive pulmonary disease (COPD) is associated with bronchial morphological changes. Metalloproteinases are thought to play a role in these structural ... [more ▼]

BACKGROUND: The course of asthma and chronic obstructive pulmonary disease (COPD) is associated with bronchial morphological changes. Metalloproteinases are thought to play a role in these structural changes. METHODS: We studied the gelatinolytic activity present in the induced sputum from 20 patients with asthma, 20 with COPD and 19 healthy controls. The assessment of gelatinolytic activity was performed by quantitative zymography, and gelatinolytic species were identified by Western blot analysis. Tissue inhibitor of metalloproteinase-1 (TIMP-1) was detected by reverse zymography and ELISA. RESULTS: From zymography, we found significantly higher gelatinolytic activity linked to pro-matrix metalloproteinase-9 (pro-MMP-9) in the sputum from asthmatics (p < 0.0001) and COPD patients (p < 0.0001) compared to the control group. Furthermore, the activated form of MMP-9 (85 kD) was found in the sputum from 60% of asthmatics and 85% of COPD patients, but was absent in that of control subjects (p < 0.0001). Importantly, although less frequently detectable than pro-MMP-9, pro- MMP-2 (72 kD) was found more frequently in asthmatics (50%) than in control subjects (5%) (p < 0. 005). We also described two unusual gelatinolytic species of 45 and 120 kD and showed that they derived from MMP-9 according to their ability to bind gelatin and anti-MMP-9 antibody. Levels of TIMP-1 were higher in asthmatics (p < 0.05) and COPD patients (p < 0.05) than in controls. CONCLUSION: Asthmatics and COPD patients display an increased gelatinolytic activity linked to MMP-2 and MMP-9 and higher levels of TIMP-1 in their sputum. [less ▲]

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See detailTheophylline Decreases Sputum Eosinophilia of Asthmatics
Louis, Renaud ULg; Bettiol, J.; Cataldo, Didier ULg et al

in International Archives of Allergy & Immunology (1999), 118(2-4, Feb-Apr), 343-4

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See detailCorrelation between Bronchoalveolar Lavage (Bal) Fluid Cell Lysate Histamine Content and Bal Fluid Eosinophil Count in Atopic and Nonatopic Asthmatics
Louis, Renaud ULg; Van Tulder, L.; Poncelet, M. et al

in International Archives of Allergy & Immunology (1997), 112(3), 309-12

We have compared the bronchoalveolar lavage fluid (BAL) cellular composition and the BAL cell lysate histamine content (fluorometric assay) in 28 stable mild to moderate asthmatics (atopic n = 18 and ... [more ▼]

We have compared the bronchoalveolar lavage fluid (BAL) cellular composition and the BAL cell lysate histamine content (fluorometric assay) in 28 stable mild to moderate asthmatics (atopic n = 18 and intrinsic n = 10) and 11 control subjects. When compared to control subjects, the whole group of asthmatics had a higher proportion of BAL eosinophils (p < 0.01) and metachromatic cells (p < 0.05). The BAL cell lysate histamine was increased in atopic (p < 0.05) and intrinsic asthmatics (p < 0.05) in comparison with control subjects. In the whole group of asthmatics, the BAL cell lysate histamine content correlated with the percentage of BAL eosinophils (r = 0.58, p < 0.01). This relationship was significant in both atopic (r = 0.48, p < 0.05) and intrinsic (r = 0.70, p < 0.05) asthmatics. For the whole group of asthmatics, both the BAL cell lysate histamine and the percentage of BAL eosinophils inversely correlated with the percent predicted FEV1 (r = -0.42, p < 0.05; r = -0.51, p < 0.05). We conclude that an increased BAL cell lysate histamine content correlates with airway eosinophilic infiltration and lung function impairment in mild to moderate atopic and intrinsic asthmatics. This suggests that BAL mast cells play a key role in recruiting eosinophils in the airways of asthmatics irrespective of the presence of an atopic status. [less ▲]

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See detailDecrease in systemic tolerance to fed ovalbumin in indomethacin-treated mice.
Louis, Edouard ULg; Franchimont, D.; Deprez, Manuel ULg et al

in International Archives of Allergy & Immunology (1996), 109(1), 21-6

The oral administration of non-steroidal anti-inflammatory drugs (NSAID) to animals induces a quick increase in intestinal permeability and secondary inflammatory lesions of the intestine. The mechanisms ... [more ▼]

The oral administration of non-steroidal anti-inflammatory drugs (NSAID) to animals induces a quick increase in intestinal permeability and secondary inflammatory lesions of the intestine. The mechanisms leading to the inflammatory lesions are hypothetical. The increased intestinal permeability could allow a greater mucosal and systemic penetration of fed antigens and bacterial products leading to an abnormal mucosal and systemic immune and inflammatory response toward these materials. We examined the effect of oral dosing with indomethacin on ovalbumin serum levels and the systemic immune response to ovalbumin in mice fed with ovalbumin. The ovalbumin serum level was higher in indomethacin-treated mice and the increase was proportional to the dose of indomethacin. It was associated with epithelial and subepithelial lesions. Moreover, the systemic humoral and, to a lesser extent, the cellular tolerance were partially abrogated in the treated mice. These findings suggest that the oral administration of indomethacin in mice induces an increased passage of fed antigen through the intestinal epithelium associated with a decrease in systemic tolerance to this antigen. The reason for this decrease remains unclear. Besides a disequilibrium between systemic and mucosal immune responses, a loss of integrity of the intestinal epithelial cells and a direct immunomodulating effect of indomethacin may also be involved. This decrease in systemic tolerance to luminal antigen could be involved in the development of NSAID enteropathy. [less ▲]

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See detailSystemic Immune Response after Rectocolonic Administration of Ovalbumin in Mice
Louis, Edouard ULg; Franchimont, D.; Lamproye, Anne ULg et al

in International Archives of Allergy & Immunology (1995), 108(1), 19-23

The aim of our study was to determine the effect of a rectocolonic preimmunization with ovalbumin on the systemic immune response induced by a subsequent subcutaneous injection of this antigen in Balb/c ... [more ▼]

The aim of our study was to determine the effect of a rectocolonic preimmunization with ovalbumin on the systemic immune response induced by a subsequent subcutaneous injection of this antigen in Balb/c mice. One rectocolonic, but not intragastric, administration of 25 mg of ovalbumin induced a detectable increase in serum anti-ovalbumin antibody level. The level reached was however much lower than after subcutaneous injection. Both intragastric and rectocolonic immunization with ovalbumin induced specific systemic cellular tolerance. However, after rectocolonic, but not intragastric, preimmunization there was no systemic humoral tolerance to this antigen. These differences in systemic immune responses after rectocolonic or intragastric administration of ovalbumin could be due to different stimulation of the systemic immune system or to differences between the colonic and small bowel mucosal immune system, which remain to be elucidated. [less ▲]

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See detailModulation of Immunological Histamine Release from Human Lung Fragments by Stem Cell Factor, Il-3, Il-5 and Gm-Csf: Comparison with Human Leukocytes
Louis, Renaud ULg; Dowlati, A.; Weber, T. et al

in International Archives of Allergy & Immunology (1994), 105(1), 18-25

Because of the importance of cytokines in the regulation of allergic inflammation, we investigated the effects of SCF, IL-3, IL-5 and GM-CSF on immunological histamine release from sensitized human lung ... [more ▼]

Because of the importance of cytokines in the regulation of allergic inflammation, we investigated the effects of SCF, IL-3, IL-5 and GM-CSF on immunological histamine release from sensitized human lung fragments as well as human leukocytes. SCF (0.2-20 ng/ml) caused a concentration-related enhancement of anti-IgE (1/100) induced histamine release from lung fragments reaching maximally 64% at 20 ng/ml. In contrast, enhancement produced by IL-5, IL-3 and GM-CSF (0.2-20 ng/ml) was quite marginal and reached at best around 20% at the higher concentration, IL-5 being slightly more effective than IL-3 and GM-CSF. Further, SCF potentiated histamine release whatever the level of immunological control whereas potentiation by IL-5 primarily occurred when the amount of histamine release induced by the immunological control ranged between 5 and 10%. SCF acted synergistically with IL-5, producing a greater enhancement of histamine release than the sum of each cytokine used alone. Both SCF and, to a lesser extent, IL-5 potentiated anti-IgE-mediated histamine release regardless of passive sensitization of lung fragments. Unlike what was observed with lung fragments, IL-3, GM-CSF and to a lesser extent IL-5, were potent enhancing agents of anti-IgE (1/2,000)-induced histamine release from leukocytes. Maximal enhancement produced by IL-3 (20 ng/ml), GM-CSF (2 ng/ml) and IL-5 (20 ng/ml) reached 92%, 78% and 61%, respectively. By contrast, SCF (0.2-20 ng/ml) was ineffective on human leukocytes.(ABSTRACT TRUNCATED AT 250 WORDS) [less ▲]

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See detailBasophil releasability in patients with hymenoptera venom allergy.
Radermecker, Maurice ULg; Leclercq, Maryse ULg; Mariz, S. D. et al

in International Archives of Allergy & Immunology (1993), 101(3), 283-7

Basophils in about 15% of subjects allergic to hymenoptera venom do not release histamine in the presence of antigen. Little is known on the basophil releasability in these patients. We therefore measured ... [more ▼]

Basophils in about 15% of subjects allergic to hymenoptera venom do not release histamine in the presence of antigen. Little is known on the basophil releasability in these patients. We therefore measured maximum percent leukocyte histamine release to antigen (Vespula venom), anti-IgE and formylmethionylphenylalanine (FMP) in 39 patients allergic to wasp venom and compared our results according to basophil responsiveness to antigen. Mean maximum percent histamine release was 39, 34 and 22%, respectively, for venom (100 ng/ml), anti-IgE (0.25 microgram/ml) and FMP (10(-4) M). The amount of histamine specifically released by venom correlated significantly with anti-IgE but not with FMP-induced histamine release. Leukocytes were unresponsive to antigen in 10 subjects. The clinical characteristics and anaphylactic symptoms of these patients were not different from those with antigen-responsive cells. Unresponsive leukocytes responded to FMP in all and to anti-IgE in 8 of the 10 subjects. Mean anti-IgE and FMP-induced histamine release were, respectively, lower and higher than those observed with leukocytes responsive to antigen (p < 0.05). In unresponsive basophils, there was a negative correlation between maximum percent anti-IgE and FMP-induced histamine release. We confirm that basophils of a minority of the subjects allergic to Vespula venom do not release histamine in the presence of antigen. The negative correlation between anti-IgE and FMP-induced histamine release in unresponsive basophils may suggest individual differences in the ratio of Fc epsilon RI and FMP receptors on the surface of basophils. [less ▲]

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