18 results on '"Gergely Tibor Kozma"'
Search Results
2. From genomes to diaries: a 3-year prospective, real-life study of ragweed-specific sublingual immunotherapy
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Lilla Tamási, Adrienne Nagy, Andras Bikov, Györgyi Zsigmond, Ibolya Czaller, Anita Farkas, Gergely Tibor Kozma, Beáta Fábos, Zsuzsanna Csoma, Maria Sasvari-Szekely, Edina Kurucz, Balint L. Balint, Zsofia Gal, Csaba Szalai, Eszter Kotyuk, Péter Antal, Gabriella Gálffy, Anikó Kurucz, Viktor Molnár, Zoltán Csontos, Magdolna Krasznai, András Gézsi, Anna Szekely, Gábor Cserta, Renata Bocskei, András Millinghoffer, and Csilla Csáki
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0301 basic medicine ,Ragweed ,medicine.medical_specialty ,Immunology ,Clinical Decision-Making ,Patient diary ,Disease ,Medical Records ,03 medical and health sciences ,0302 clinical medicine ,Quality of life (healthcare) ,medicine ,Hypersensitivity ,Immunology and Allergy ,Humans ,Patient Reported Outcome Measures ,Prospective Studies ,Precision Medicine ,Intensive care medicine ,Electronic Data Processing ,Sublingual Immunotherapy ,Genome ,biology ,business.industry ,Medical record ,Data Collection ,Allergens ,Antigens, Plant ,Precision medicine ,biology.organism_classification ,030104 developmental biology ,Phenotype ,030228 respiratory system ,Oncology ,Observational study ,Personalized medicine ,Ambrosia ,business - Abstract
During the last decades, the prevalence of allergy has dramatically increased. Allergen-specific immunotherapy is the only currently available medical intervention that has the potential to affect the natural course of the disease, but there are still many questions and unmet needs hindering its widespread use to fulfill its treatment potential and maximize its benefits for the society. To provide a comprehensive phenome-wide overview in sublingual immunotherapy, using ragweed allergy as a target, we planned and carried out a longitudinal, prospective, observational, open-label study (DesensIT). In this paper we present challenges of using deep and comprehensive phenotypes embracing biological, clinical and patient-reported outcomes in allergen-specific immunotherapy and show how we designed the DesensIT project to optimize data collection, processing and evaluation.
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- 2017
3. Infusion Reactions Associated with the Medical Application of Monoclonal Antibodies: The Role of Complement Activation and Possibility of Inhibition by Factor H
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Tamas Fulop, Tamás Mészáros, Mihály Józsi, Gergely Tibor Kozma, and Janos Szebeni
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lcsh:Immunologic diseases. Allergy ,0301 basic medicine ,CARPA ,medicine.drug_class ,Immunology ,Review ,infusion reaction ,Monoclonal antibody ,03 medical and health sciences ,0302 clinical medicine ,Drug Discovery ,Immunology and Allergy ,Medicine ,complement ,Pseudoallergic reaction ,Monoclonal antibody therapy ,complement activation ,Innate immune system ,business.industry ,monoclonal antibody therapy ,Pseudoallergy ,factor H ,medicine.disease ,pseudoallergic reaction ,3. Good health ,Complement system ,030104 developmental biology ,030220 oncology & carcinogenesis ,Factor H ,Alternative complement pathway ,hypersensitivity ,lcsh:RC581-607 ,business - Abstract
Human application of monoclonal antibodies (mAbs), enzymes, as well as contrast media and many other particulate drugs and agents referred to as "nanomedicines", can initiate pseudoallergic hypersensitivity reactions, also known as infusion reactions. These may in part be mediated by the activation of the complement system, a major humoral defense system of innate immunity. In this review, we provide a brief outline of complement activation-related pseudoallergy (CARPA) in general, and then focus on the reactions caused by mAb therapy. Because the alternative pathway of complement activation may amplify such adverse reactions, we highlight the potential use of complement factor H as an inhibitor of CARPA.
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- 2018
4. Contents Vol. 151, 2010
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Jesús Jurado-Palomo, Guro Gafvelin, Tiiu Saarne, Wei Guo, Philippe-Jean Bousquet, Hye Yung Yum, David H. Broide, Gergely Tibor Kozma, Laura Gilmartin, Salvatore Metafora, Salvatore De Maria, Torsten Zuberbier, András Szabó, Yang Zhao, Janet M. Oliver, Beáta Szebeni, Zsolt István Komlósi, Ana María Fiandor-Román, F. Al-Maskari, S. Al-Hammadi, Irina Bobolea, Amato de Paulis, Hans Grönlund, Santiago Quirce, Maria Cartenì, Tereassa Archibeque, Massimo Triggiani, Mark Schuyler, Nella Prevete, Dae Jin Song, György Losonczy, Jiong Yang, Éva Pállinger, Lajos Kovács, Ádám Vannay, George N. Konstantinou, Csaba Ádori, Jae Youn Cho, Cristina Y. Pascual, Gianpietro Ravagnan, Ya-dong Gao, R. Bernsen, Raffaele Ragone, Myung Goo Min, Lorena Diehl, Sofía Sánchez-Pastor, Gianni Marone, Christy A. Tarleton, Krisztina Rusai, Clifford Qualls, Francesca Wanda Rossi, Erna Sziksz, Marina Miller, Nikolaos G. Papadopoulos, Bridget S. Wilson, Marianne van Hage, and Vittoria Metafora
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Immunology ,Immunology and Allergy ,General Medicine ,Biology - Published
- 2010
5. Galectin-9 in Allergic Airway Inflammation and Hyper-Responsiveness in Mice
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György Losonczy, Zsolt István Komlósi, Beáta Szebeni, András Szabó, Lajos Kovács, Éva Pállinger, Ádám Vannay, Erna Sziksz, Csaba Ádori, Gergely Tibor Kozma, and Krisztina Rusai
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Allergy ,Ovalbumin ,Galectins ,Immunology ,Anti-Inflammatory Agents ,Inflammation ,Granulocyte ,Dexamethasone ,Allergic inflammation ,Mice ,Cell Movement ,Animals ,Immunology and Allergy ,Medicine ,Inducer ,Methacholine Chloride ,Galectin ,Mice, Inbred BALB C ,business.industry ,General Medicine ,Allergens ,Eosinophil ,medicine.disease ,Asthma ,Respiratory Function Tests ,Disease Models, Animal ,medicine.anatomical_structure ,Microscopy, Fluorescence ,Apoptosis ,Cytokines ,Female ,medicine.symptom ,business ,Bronchoalveolar Lavage Fluid ,Granulocytes - Abstract
Background: Galectin-9 (Gal-9) is a member of the growing family of β-galactoside-binding lectins. Gal-9 is an eosinophil chemoattractant and inducer of Th1 cell apoptosis. These effects suggest its potential role in the pathogenesis of asthma. Our aim was to study the expression of Gal-9 in an ovalbumin (OVA)-induced mouse model of allergic asthma. Methods: To investigate the significance of Gal-9 in allergic inflammation and airway hyperresponsiveness (AHR), a group of BALB/c mice was sensitized and challenged with OVA (GOVA). Another group of animals was allergized with OVA and also treated with dexamethasone (DEX) (GOVA+DEX). The control group (GPBS) received phosphate-buffered saline instead of OVA as placebo. Airway reactivity to intravenous methacholine was assessed. Results: The percentage of Gal-9-positive cells and their intracellular Gal-9 content and Th1/Th2 cytokine levels in the bronchoalveolar lavage (BAL) were determined by flow cytometry. Gal-9 mRNA expression and protein level were measured in the lung tissue by real-time RT-PCR and Western blot. In GOVA mice, airway inflammation and mucus hypersecretion developed. DEX treatment inhibited the main features of experimental asthma. The number of Gal-9-positive lymphocytes, eosinophil and neutrophil granulocytes and the levels of Th2 cytokines were higher in the BAL of GOVA compared to GPBS or GOVA+DEX mice. Moreover, Gal-9 protein level was elevated in the lungs of GOVA mice. Conclusions: These results suggest that Gal-9 plays a role as a mediator contributing to the development of allergic airway inflammation. Gal-9 may serve as a recruiter of eosinophil granulocytes and promoter of Th2 dominance.
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- 2009
6. Variable association of complement activation by rituximab and paclitaxel in cancer patients in vivo and in their screening serum in vitro with clinical manifestations of hypersensitivity: a pilot study
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András Rosta, Zsoka Weiszhar, Rudolf Urbanics, Janos Szebeni, Tamás Mészáros, László Rosivall, Gergely Tibor Kozma, and Tamás Schneider
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business.industry ,Immunogenicity ,Biomedical Engineering ,Medicine (miscellaneous) ,Cancer ,Bioengineering ,medicine.disease ,In vitro ,Complement system ,chemistry.chemical_compound ,Paclitaxel ,chemistry ,In vivo ,Immunology ,medicine ,Rituximab ,Physical and Theoretical Chemistry ,business ,Anaphylaxis ,medicine.drug - Abstract
To explore the role of complement (C) activation in the hypersensitivity reactions (HSRs) to some anticancer drugs, as well as the use of the C activation biomarkers (C
- Published
- 2015
7. Pediatric Asthmatic Patients Have Low Serum Levels of Monocyte Chemoattractant Protein-1
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Csaba Szalai, Gergely Tibor Kozma, Marton Keszei, Károly Radosits, Adrienne Nagy, A. Falus, and Gergely Tölgyesi
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Male ,Pulmonary and Respiratory Medicine ,Chemokine ,Adolescent ,Enzyme-Linked Immunosorbent Assay ,Inflammation ,Severity of Illness Index ,Atopy ,Polymorphism (computer science) ,Genotype ,Humans ,Immunology and Allergy ,Medicine ,Allele ,Child ,Chlamydophila Infections ,Glucocorticoids ,Genotyping ,Chemokine CCL2 ,Asthma ,Polymorphism, Genetic ,biology ,business.industry ,medicine.disease ,Child, Preschool ,Pediatrics, Perinatology and Child Health ,Immunology ,biology.protein ,Female ,medicine.symptom ,business - Abstract
Serum levels of MCP-1 were measured in children with and without asthma in order to determine a possible correlation between the MCP-1-2518A/G polymorphism, serum levels of MCP-1 and asthma. Two groups of subjects -160 children with asthma and 158 healthy children were screened with a PCR-based genotyping assay. Serum MCP-1 level was measured by ELISA. The -2518G allele occurred at a significantly higher frequency in asthmatic children than in controls. The mean serum MCP-1 level was significantly lower in the asthmatic than in the control children. There was no significant association between the MCP-1 genotypes and the serum MCP-1 levels.
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- 2006
8. Polymorphism in the gene regulatory region of MCP-1 is associated with asthma susceptibility and severity
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T. Szabó, Adrienne Nagy, Csaba Szalai, Dóra Krikovszky, Gergely Tibor Kozma, Ágnes Bojszkó, and András Falus
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Allergy ,Pathophysiology of asthma ,Adolescent ,Genotype ,Immunology ,Regulatory Sequences, Nucleic Acid ,Polymorphism, Single Nucleotide ,Cohort Studies ,Atopy ,Leukocyte Count ,Gene Frequency ,Immunopathology ,medicine ,Humans ,Immunology and Allergy ,Genetic Predisposition to Disease ,Allele ,Child ,Chemokine CCL5 ,Genotyping ,Chemokine CCL2 ,Asthma ,Hungary ,Polymorphism, Genetic ,business.industry ,Infant ,Eosinophil ,medicine.disease ,Eosinophils ,medicine.anatomical_structure ,Child, Preschool ,business - Abstract
Chemokines play an important role in the pathophysiology of asthma and allergy. Recently, polymorphisms in the gene regulatory region of monocyte chemoattractant protein 1 (MCP-1) and in the promoter region of RANTES have been found; these polymorphisms increase the expression of the chemokines.We investigated whether the presence of the polymorphisms was associated with atopy or asthma and whether these alleles influenced the severity of asthma in affected individuals.Three groups of subjects-160 children with asthma (disease severity being classified according to the Global Initiative for Asthma guidelines, modified for children), 151 children with nonasthmatic but allergic phenotype, and 303 children without allergic or asthmatic disorders-were screened with a PCR-based assay for genotyping.The frequency of the -2518G polymorphism in the gene regulatory region of MCP-1 was significantly higher in asthmatic children than in controls (P.001; odds ratio [OR] = 2.0 [1.4-2.6]) and nonasthmatic atopic children (P.001; OR = 2.0 [1.4-2.9]). The MCP-1 G/G genotype correlated with asthma severity. In asthmatic children, the MCP-1 -2518G allele was also associated with an increased blood eosinophil level. The promoter polymorphisms in the RANTES gene did not have a detectable effect on the susceptibility to asthma or allergy or on the blood eosinophil count.In this cohort of children, there are associations between carrying G at -2518 of the MCP-1 gene regulatory region and the presence of asthma as well as between asthma severity and homozygosity for the G allele. In asthmatic children, the MCP-1 -2518G polymorphism correlated with increased eosinophil levels. This variant of MCP-1 might belong to the predictor gene set for asthma.
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- 2001
9. CCR5Δ32 mutation, Mycoplasma pneumoniae infection, and asthma
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Ágnes F. Semsei, Adrienne Nagy, Gergely Tibor Kozma, András Falus, Csaba Szalai, Károly Radosits, Gergely Tölgyesi, Ildikó Ungvári, and Marton Keszei
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Mice, Knockout ,Mycoplasma pneumoniae ,Receptors, CCR5 ,business.industry ,Immunology ,medicine.disease ,medicine.disease_cause ,Virology ,Asthma ,Cohort Studies ,Mice ,Chronic Disease ,Pneumonia, Mycoplasma ,Mutation (genetic algorithm) ,medicine ,Animals ,Humans ,Immunology and Allergy ,Genetic Predisposition to Disease ,Child ,business ,Chemokine CCL5 ,Sequence Deletion - Published
- 2007
10. Seasonal changes of proapoptotic soluble Fas ligand level in allergic rhinitis combined with asthma
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Györgyi Mezei, Gergely Tibor Kozma, Endre Cserháti, Erika Héninger, Zsuzsanna Sepler, and Magdolna Lévay
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Ragweed ,Male ,Allergy ,Fas Ligand Protein ,Immunology ,Apoptosis ,Immunoglobulin E ,Fas ligand ,Allergic inflammation ,Immunopathology ,Forced Expiratory Volume ,Immunology and Allergy ,Ambrosia ,Medicine ,Humans ,Child ,Asthma ,Membrane Glycoproteins ,biology ,business.industry ,Rhinitis, Allergic, Seasonal ,biology.organism_classification ,medicine.disease ,Eosinophils ,Pediatrics, Perinatology and Child Health ,Tumor Necrosis Factors ,biology.protein ,Pollen ,Female ,Seasons ,business - Abstract
The function of apoptosis is to eliminate unnecessary or dangerous cells. The balance between production and death is important in the control of cell numbers within physiological ranges. Cells involved in allergic reactions may have altered apoptosis. The aim of this study was to examine the seasonal changes of programmed cell death in children with pollen allergy. We measured serum levels of soluble Fas (sFas) and soluble Fas ligand (sFasL), and examined whether there was any correlation between soluble apoptosis markers and development of asthma and or rhinitis in children with pollen allergy. We examined two groups of patients with ragweed pollen allergy. The first group consisted of 17 children with 'rhinitis only'. The second group consisted of 16 children with 'asthma + rhinitis'. For seasonal analysis we pooled the two groups and termed this the 'ragweed sensitive' group (n = 33, 5-18 yr, 25 boys, eight girls). Measurements (sFas and sFasL) were taken during the ragweed pollen allergy season, while control measurements were performed during the symptom-free period. There was no difference in sFas levels measured during and after [1941 +/- 68, 1963 +/- 83 pg/ml (mean+/-s.e.m, respectively)] the pollen season in the 'ragweed sensitive' group. The sFasL level showed seasonal change, which was significantly higher (p = 0.0086) in the symptomatic period compared to the symptom-free state (99 +/- 13 and 53 +/- 16 pg/ml, respectively). There was a difference between the 'rhinitis only' and the 'asthma + rhinitis' groups in the measured parameters of apoptosis. Children having allergic rhinitis combined with asthma had a significantly (p = 0.03) higher sFas level in the symptom-free state than the 'rhinitis only' group did (2115 +/- 156 and 1820 +/- 52 pg/ml, respectively). During the allergic symptom state the sFasL level of the 'asthma + rhinitis' group was significantly higher (p = 0.025) than that of the 'rhinitis only' group (125 +/- 20 and 75 +/- 14 pg/ml, respectively). In conclusion, the increased level of sFasL during the pollen season may signal its role in the pathogenesis of allergic airway diseases. There was no seasonal change in sFas levels in the examined ragweed allergic group, however in the symptomatic period we observed a diminished level of antiapoptotic factor (sFas) and an elevated level of proapoptotic factor (sFasL) if there was a combined disease with pollen allergic asthma. We suggest that there is a deviation in the apoptotic reaction in children that may increase the seasonal allergic inflammation.
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- 2006
11. Lipopolysaccharide exposure makes allergic airway inflammation and hyper-responsiveness less responsive to dexamethasone and inhibition of iNOS
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Zsolt István Komlósi, Bartos B, Lilla Tamási, Andrea Nagy, Marta Orosz, E. Szoko, Tamás Tábi, Pál Magyar, György Losonczy, Gergely Tibor Kozma, and Pozsonyi E
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Lipopolysaccharides ,Allergy ,Ovalbumin ,medicine.medical_treatment ,Immunology ,Drug Resistance ,Nitric Oxide Synthase Type II ,Inflammation ,Dexamethasone ,Nitric oxide ,chemistry.chemical_compound ,Mice ,medicine ,Immunology and Allergy ,Animals ,Pulmonary Eosinophilia ,Glucocorticoids ,Nitrites ,Mice, Inbred BALB C ,Nitrates ,medicine.diagnostic_test ,biology ,business.industry ,respiratory system ,Eosinophil ,medicine.disease ,Asthma ,respiratory tract diseases ,Bronchoalveolar lavage ,Cytokine ,medicine.anatomical_structure ,chemistry ,biology.protein ,Cytokines ,Female ,Imines ,medicine.symptom ,Bronchial Hyperreactivity ,business ,medicine.drug - Abstract
Summary Allergic airway disease can be refractory to anti-inflammatory treatment, whose cause is unclarified. Therefore, in the present experiment, we have tested the hypothesis that co-exposure to lipopolysacharide (Lps) and allergen results in glucocorticoid-resistant eosinophil airway inflammation and hyper-responsiveness (AHR). Ovalbumin (Ova)-sensitized BALB/c mice were primed with 10 μg intranasal Lps 24 h before the start of Ova challenges (20 min on 3 consecutive days). Dexamethasone (5 mg/kg/day) was given on the last 2 days of Ova challenges. AHR, cellular build-up, cytokine and nitrite concentrations of bronchoalveolar lavage fluid (BALF) and lung histology were examined. To assess the role of iNOS-derived NO in airway responsiveness, mice were treated with a selective inhibitor of this enzyme (1400W) 2 h before AHR measurements. More severe eosinophil inflammation and higher nitrite formation were found in Lps-primed than in non-primed allergized mice. After Lps priming, AHR and concentrations of T-helper type 2 cytokines in BALF were decreased, but still remained significantly higher than in controls. Eosinophil inflammation was partially, while nitrite production and AHR were observed to be largely dexamethasone resistant in Lps-primed allergized animals. 1400W effectively and rapidly diminished the AHR in Ova-sensitized and challenged mice, but failed to affect it after Lps priming plus allergization. In conclusion, Lps inhalation may exaggerate eosinophil inflammation and reduce responsiveness to anti-inflammatory treatment in allergic airway disease.
- Published
- 2006
12. The development of asthma in children infected with Chlamydia pneumoniae is dependent on the modifying effect of mannose-binding lectin
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Marton Keszei, Gergely Tibor Kozma, András Treszl, Csaba Szalai, András Falus, and Adrienne Nagy
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Male ,Allergy ,Adolescent ,Genotype ,Immunology ,Enzyme-Linked Immunosorbent Assay ,Mannose-Binding Lectin ,Polymerase Chain Reaction ,Recurrence ,medicine ,Immunology and Allergy ,Humans ,Chlamydiaceae ,Genetic Predisposition to Disease ,Risk factor ,Child ,Chlamydophila Infections ,Alleles ,Mannan-binding lectin ,Asthma ,Chlamydia ,biology ,Genetic Variation ,Odds ratio ,Chlamydophila pneumoniae ,biology.organism_classification ,medicine.disease ,respiratory tract diseases ,Case-Control Studies ,Child, Preschool ,Chronic Disease ,Female ,Polymorphism, Restriction Fragment Length - Abstract
Background Although several studies found associations between infection with Chlamydia pneumoniae and asthma, these were mainly restricted to the exacerbation of the symptoms in adults with known asthma. Data about the role of C pneumoniae in the initiation and development of asthma in children are controversial. Objective We investigated the role of C pneumoniae infection in 139 children with asthma, comparing them with 174 healthy control subjects. Furthermore, we studied the modifying effect of mannose-binding lectin (MBL) variant alleles on the susceptibility to asthma in children infected with C pneumoniae . Methods C pneumoniae –specific antibodies were measured by means of ELISA, and MBL genotypes were determined by means of PCR-RFLP. Results There were no significant differences in the percentage of children with positive results for C pneumoniae –specific antibodies between patients and control subjects. Among asthmatic children carrying variant MBL alleles, there were significantly more patients with positive results for C pneumoniae –specific IgG than among control children with variant MBL genotypes (63.7% vs 40.7% of asthmatic vs control children, respectively; odds ratio adjusted for age and sex, 2.21; 95% CI, 1.10-4.41; P = .02). Infected children with variant MBL alleles were found to have a higher risk of asthma development than infected children with normal MBL genotype. This risk was especially high in children with chronic or recurrent infection (positive results for both IgA and IgG; adjusted odds ratio, 5.38; 95% CI, 1.75-14.36; P = .01), but no increased risk was seen in children with current C pneumoniae infection (positive results for IgM). Conclusion This study indicates the important role of variant MBL alleles in the susceptibility to asthma in children infected with C pneumoniae. (J Allergy Clin Immunol 2003;112:729-34.)
- Published
- 2003
13. Histamine deficiency in gene-targeted mice strongly reduces antigen-induced airway hyper-responsiveness, eosinophilia and allergen-specific IgE
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György Losonczy, Zsolt István Komlósi, Pál Magyar, Judith Appel, Csaba Szalai, Éva Pállinger, András Falus, Gergely Tibor Kozma, Edit I. Buzás, T. Szabó, and Marton Keszei
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Neutrophils ,Histidine Decarboxylase ,Immunoglobulin E ,chemistry.chemical_compound ,Leukocyte Count ,Mice ,Immunology and Allergy ,Eosinophilia ,Lung ,Methacholine Chloride ,Oligonucleotide Array Sequence Analysis ,Mice, Knockout ,Mice, Inbred BALB C ,biology ,Histocytochemistry ,Degranulation ,General Medicine ,respiratory system ,Mast cell ,Histidine decarboxylase ,Plethysmography ,medicine.anatomical_structure ,Data Interpretation, Statistical ,Cytokines ,Female ,medicine.symptom ,Chemokines ,Bronchoalveolar Lavage Fluid ,Histamine ,medicine.medical_specialty ,Ovalbumin ,Immunology ,Enzyme-Linked Immunosorbent Assay ,Bronchial Provocation Tests ,Interferon-gamma ,Internal medicine ,medicine ,Animals ,Histamine H4 receptor ,Analysis of Variance ,Gene Expression Profiling ,Eosinophil ,Asthma ,Eosinophils ,Endocrinology ,chemistry ,biology.protein ,Immunization ,Interleukin-4 - Abstract
Histamine is an important mediator released from activated mast cells provoked by allergen and has a substantial role in the pathophysiology of asthma. However, several lines of evidence indicate that histamine could also have important functions in the regulation of basic cell biological processes. We have used histidine decarboxylase gene-targeted (HDC-KO) mice, lacking histamine, to investigate the effect of histamine deficiency in an animal model of asthma. Our previous investigations revealed that HDC-KO mice had fewer mast cells with reduced granular content and defective degranulation characteristics. Ovalbumin (OVA)-sensitized and challenged HDC-KO mice had significantly reduced airway hyper-responsiveness, lung inflammation, bronchoalveolar lavage eosinophilia, and OVA-specific IgE compared with congenic wild-type littermates treated in the same way. Comparing the expression profiles of cytokines, the levels of IL-1alpha, IL-1beta, IL-4, IL-5, IL-6 and IFN-gamma were significantly lower in the HDC-KO mice in asthmatic late phase, indicating a significantly altered immune response to OVA provocation and challenge. Evaluation of chemokine gene expression revealed that OVA treatment caused elevation of both T(h)1- and T(h)2-type chemokines in wild-type mice, while the chemokine expression was polarized toward a T(h)1 response in HDC-KO mice. According to our results we can suggest that the possible causes of the reduced asthma symptoms in the HDC-KO mice may be the imperfect mast and eosinophil cell system, and an altered immune response to OVA provocation and challenge.
- Published
- 2003
14. Lack of association between atopic eczema/dermatitis syndrome and polymorphisms in the promoter region of RANTES and regulatory region of MCP-1
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András Falus, Adrienne Nagy, Csaba Szalai, Gergely Tibor Kozma, Dóra Krikovszky, T. Szabó, and Ágnes Bojszkó
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Male ,Allergy ,Adolescent ,Genotype ,Immunology ,Statistics as Topic ,Child Welfare ,Regulatory Sequences, Nucleic Acid ,Dermatitis, Atopic ,Atopy ,Leukocyte Count ,Gene Frequency ,White blood cell ,Immunopathology ,Germany ,medicine ,Prevalence ,Immunology and Allergy ,Humans ,Allele ,Child ,Promoter Regions, Genetic ,Chemokine CCL5 ,Chemokine CCL2 ,Polymorphism, Genetic ,business.industry ,Atopic dermatitis ,Eosinophil ,Immunoglobulin E ,medicine.disease ,Eosinophils ,medicine.anatomical_structure ,Child, Preschool ,Female ,business - Abstract
Background: Chemokines play an important role in the pathophysiology of atopic eczema/dermatitis syndrome (AEDS) and allergy. Recently polymorphisms in the promoter region of RANTES (regulated on activation normal T cell expressed and secreted) and in the gene regulatory region of MCP-1 (monocyte chemoattractant protein-1) have been found, which increase the expression of these chemokines. The − 403A allele of the RANTES promoter region was found associated with AEDS in German children. We investigated whether the presence of these polymorphisms was associated with AEDS or allergy in Hungarian children. Methods: One hundred and twenty-eight children with AEDS, 102 allergic children without AEDS and 303 children of comparable ages without allergic disorders were screened for genotype with a PCR-based assay. Results: There were no significant differences in the frequency of these polymorphisms, or in the distribution of genotypes between the groups. The total IgE concentration, the white blood cell count and the blood eosinophil cell count did not differ between the genotypes. Conclusion: In this cohort of Hungarian children there was no association between − 28G, and − 403A alleles in the RANTES promoter, − 2518G polymorphism in the distal regulatory region of the MCP-1 and AEDS, or allergy.
- Published
- 2002
15. Subject Index Vol. 151, 2010
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Ádám Vannay, David H. Broide, Myung Goo Min, Torsten Zuberbier, Salvatore De Maria, Gergely Tibor Kozma, Guro Gafvelin, Lajos Kovács, Philippe-Jean Bousquet, Laura Gilmartin, Jesús Jurado-Palomo, Beáta Szebeni, Dae Jin Song, György Losonczy, Gianni Marone, Amato de Paulis, Ya-dong Gao, Hans Grönlund, Tiiu Saarne, Christy A. Tarleton, R. Bernsen, George N. Konstantinou, Santiago Quirce, Tereassa Archibeque, Jae Youn Cho, Irina Bobolea, Zsolt István Komlósi, Vittoria Metafora, Massimo Triggiani, Nella Prevete, Gianpietro Ravagnan, Jiong Yang, Éva Pállinger, Krisztina Rusai, Csaba Ádori, Janet M. Oliver, Marina Miller, Cristina Y. Pascual, Ana María Fiandor-Román, Mark Schuyler, Bridget S. Wilson, Francesca Rossi, Lorena Diehl, Sofía Sánchez-Pastor, András Szabó, S. Al-Hammadi, F. Al-Maskari, Yang Zhao, Raffaele Ragone, Wei Guo, Clifford Qualls, Nikolaos G. Papadopoulos, Hye Yung Yum, Marianne van Hage, Salvatore Metafora, Erna Sziksz, and Maria Cartenì
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Index (economics) ,Immunology ,Statistics ,Immunology and Allergy ,Subject (documents) ,General Medicine ,Psychology - Published
- 2010
16. No association between asthma or allergy and the CCR5Delta 32 mutation
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Csaba Szalai, Gergely Tibor Kozma, Adrienne Nagy, András Falus, Dóra Krikovszky, and Ágnes Bojszkó
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Allergy ,Adolescent ,Genotype ,Receptors, CCR5 ,Atopy ,Gene Frequency ,immune system diseases ,Hypersensitivity ,Humans ,Medicine ,Allele ,Child ,Allele frequency ,Asthma ,business.industry ,Wild type ,Infant ,Eosinophil ,medicine.disease ,respiratory tract diseases ,medicine.anatomical_structure ,Child, Preschool ,Mutation ,Pediatrics, Perinatology and Child Health ,Immunology ,Original Article ,business - Abstract
Aims: To investigate whether the presence of the CCR5Δ32 allele was associated with atopy or asthma. Methods: A total of 118 children with asthma, 145 children with non-asthmatic, but allergic phenotype, and 303 children without allergic or asthmatic disorders were studied. Results: There were no significant differences in the frequency of CCR5Δ32, or in the distributions of genotypes between the groups. The relative eosinophil blood count was slightly lower in patients with heterozygous genotype, than in patients with wild type genotype. Conclusion: No association was found between the susceptibility of allergy or asthma and the functional deficient CCR5Δ32 allele.
- Published
- 2002
17. Anti-PEG antibodies: Properties, formation, testing and role in adverse immune reactions to PEGylated nano-biopharmaceuticals
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Taro Shimizu, Janos Szebeni, Gergely Tibor Kozma, and Tatsuhiro Ishida
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Drug targeting ,Drug ,Hypersensitivity reactions ,media_common.quotation_subject ,Complement ,Pharmaceutical Science ,Biologicals ,Adverse drug reactions (ADRs) ,02 engineering and technology ,Antibodies ,Polyethylene Glycols ,03 medical and health sciences ,Therapeutic index ,Pharmacokinetics ,Anti-drug antibodies ,Animals ,Humans ,Medicine ,Adverse effect ,030304 developmental biology ,media_common ,0303 health sciences ,biology ,business.industry ,Immunogenicity ,technology, industry, and agriculture ,021001 nanoscience & nanotechnology ,Nanomedicines ,C activation-related pseudoallergy (CARPA) ,Nanomedicine ,Targeted drug delivery ,Liposomes ,Drug delivery ,Immunology ,biology.protein ,Biological Assay ,Accelerated blood clearance (ABC) ,Antibody ,0210 nano-technology ,business - Abstract
Conjugation of polyethylene glycols (PEGs) to proteins or drug delivery nanosystems is a widely accepted method to increase the therapeutic index of complex nano-biopharmaceuticals. Nevertheless, these drugs and agents are often immunogenic, triggering the rise of anti-drug antibodies (ADAs). Among these ADAs, anti-PEG IgG and IgM were shown to account for efficacy loss due to accelerated blood clearance of the drug (ABC phenomenon) and hypersensitivity reactions (HSRs) entailing severe allergic symptoms with occasionally fatal anaphylaxis. In addition to recapitulating the basic information on PEG and its applications, this review expands on the physicochemical factors influencing its immunogenicity, the prevalence, features, mechanism of formation and detection of anti-PEG IgG and IgM and the mechanisms by which these antibodies (Abs) induce ABC and HSRs. In particular, we highlight the in vitro, animal and human data attesting to anti-PEG Ab-induced complement (C) activation as common underlying cause of both adverse effects. A main message is that correct measurement of anti-PEG Abs and individual proneness for C activation might predict the rise of adverse immune reactions to PEGylated drugs and thereby increase their efficacy and safety.
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18. Mini-Factor H Modulates Complement-Dependent IL-6 and IL-10 Release in an Immune Cell Culture (PBMC) Model: Potential Benefits Against Cytokine Storm
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Gergely Tibor Kozma, Tamás Mészáros, Tamás Bakos, Mark Hennies, Dániel Bencze, Barbara Uzonyi, Balázs Győrffy, Edward Cedrone, Marina A. Dobrovolskaia, Mihály Józsi, and János Szebeni
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0301 basic medicine ,medicine.medical_treatment ,immune stimulation ,Immunology ,zymosan ,Proinflammatory cytokine ,03 medical and health sciences ,0302 clinical medicine ,Immune system ,complement activation/inhibition ,medicine ,Immunology and Allergy ,Humans ,Anaphylatoxin ,Complement Activation ,Original Research ,Innate immune system ,Chemistry ,Interleukin-6 ,SARS-CoV-2 ,Models, Immunological ,COVID-19 ,cytokine release syndrome ,anaphylatoxins ,RC581-607 ,medicine.disease ,factor H ,whole blood assay ,Complement system ,Interleukin-10 ,Cytokine release syndrome ,030104 developmental biology ,Cytokine ,030220 oncology & carcinogenesis ,Complement Factor H ,Leukocytes, Mononuclear ,Immunologic diseases. Allergy ,Cytokine storm - Abstract
Cytokine storm (CS), an excessive release of proinflammatory cytokines upon overactivation of the innate immune system, came recently to the focus of interest because of its role in the life-threatening consequences of certain immune therapies and viral diseases, including CAR-T cell therapy and Covid-19. Because complement activation with subsequent anaphylatoxin release is in the core of innate immune stimulation, studying the relationship between complement activation and cytokine release in an in vitro CS model holds promise to better understand CS and identify new therapies against it. We used peripheral blood mononuclear cells (PBMCs) cultured in the presence of autologous serum to test the impact of complement activation and inhibition on cytokine release, testing the effects of liposomal amphotericin B (AmBisome), zymosan and bacterial lipopolysaccharide (LPS) as immune activators and heat inactivation of serum, EDTA and mini-factor H (mfH) as complement inhibitors. These activators induced significant rises of complement activation markers C3a, C4a, C5a, Ba, Bb, and sC5b-9 at 45 min of incubation, with or without ~5- to ~2,000-fold rises of IL-1α, IL-1β, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12, IL-13 and TNFα at 6 and 18 h later. Inhibition of complement activation by the mentioned three methods had differential inhibition, or even stimulation of certain cytokines, among which effects a limited suppressive effect of mfH on IL-6 secretion and significant stimulation of IL-10 implies anti-CS and anti-inflammatory impacts. These findings suggest the utility of the model for in vitro studies on CS, and the potential clinical use of mfH against CS.
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