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1. Searching for Genetic Biomarkers for Hereditary Angioedema Due to C1-Inhibitor Deficiency (C1-INH-HAE)

Author

Faidra Parsopoulou, Gedeon Loules, Maria Zamanakou, Dorottya Csuka, Agnes Szilagyi, Maria Kompoti, Grzegorz Porebski, Fotis Psarros, Markus Magerl, Anna Valerieva, Maria Staevska, Krystyna Obtulowicz, Marcus Maurer, Matthaios Speletas, Henriette Farkas, and Anastasios E. Germenis

Subjects
C1-inhibitor deficiency, genetic biomarkers, functional variants, hereditary angioedema, long-term prophylaxis, next-generation sequencing, Immunologic diseases. Allergy, RC581-607
Abstract

Existing evidence indicates that modifier genes could change the phenotypic outcome of the causal SERPING1 variant and thus explain the expression variability of hereditary angioedema due to C1-inhibitor deficiency (C1-INH-HAE). To further examine this hypothesis, we investigated the presence or absence of 18 functional variants of genes encoding proteins involved in the metabolism and function of bradykinin, the main mediator of C1-INH-HAE attacks, in relation to three distinct phenotypic traits of patients with C1-INH-HAE, i.e., the age at disease onset, the need for long-term prophylaxis (LTP), and the severity of the disease. Genetic analyses were performed by a validated next-generation sequencing platform. In total, 233 patients with C1-INH-HAE from 144 unrelated families from five European countries were enrolled in the study. Already described correlations between five common functional variants [F12-rs1801020, KLKB1-rs3733402, CPN1-rs61751507, and two in SERPING1 (rs4926 and rs28362944)] and C1-INH-HAE severity were confirmed. Furthermore, significant correlations were found between either the age at disease onset, the LTP, or the severity score of the disease and a series of other functional variants (F13B-rs6003, PLAU-rs2227564, SERPINA1-rs28929474, SERPINA1-rs17580, KLK1-rs5515, SERPINE1-rs6092, and F2-rs1799963). Interestingly, correlations uncovered in the entire cohort of patients were different from those discovered in the cohort of patients carrying missense causal SERPING1 variants. Our findings indicate that variants other than the SERPING1 causal variants act as independent modifiers of C1-INH-HAE severity and could be tested as possible prognostic biomarkers.

Published
2022
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2. A novel deep intronic SERPING1 variant as a cause of hereditary angioedema due to C1-inhibitor deficiency

Author

Sofia Vatsiou, Maria Zamanakou, Gedeon Loules, Fotis Psarros, Faidra Parsopoulou, Dorottya Csuka, Anna Valerieva, Maria Staevska, Grzegorz Porebski, Krystyna Obtulowicz, Markus Magerl, Marcus Maurer, Matthaios Speletas, Henriette Farkas, and Anastasios E. Germenis

Subjects
C1-inhibitor deficiency, Hereditary angioedema, Intronic mutations, Next-generation sequencing, SERPING1 gene, Immunologic diseases. Allergy, RC581-607
Abstract

Background: In about 5% of patients with hereditary angioedema due to C1-inhibitor deficiency (C1-INH-HAE) no mutation in the SERPING1 gene is detected. Methods: C1-INH-HAE cases with no mutation in the coding region of SERPING1 after conventional genotyping were examined for defects in the intronic or untranslated regions of the gene. Using a next-generation sequencing (NGS) platform targeting the entire SERPING1, 14 unrelated C1-INH-HAE patients with no detectable mutations in the coding region of the gene were sequenced. Detected variants with a global minor allele frequency lower than the frequency of C1-INH-HAE (0.002%), were submitted to in silico analysis using ten different bioinformatics tools. Pedigree analysis and examination of their pathogenic effect on the RNA level were performed for filtered in variants. Results: In two unrelated patients, the novel mutation c.-22-155G > T was detected in intron 1 of the SERPING1 gene by the use NGS and confirmed by Sanger sequencing. All bioinformatics tools predicted that the variant causes a deleterious effect on the gene and pedigree analysis showed its co-segregation with the disease. Degradation of the mutated allele was demonstrated by the loss of heterozygosity on the cDNA level. According to the American College of Medical Genetics and Genomics 2015 guidelines the c.-22-155G > T was curated as pathogenic. Conclusions: For the first time, a deep intronic mutation that was detected by NGS in the SERPING1 gene, was proven pathogenic for C1-INH-HAE. Therefore, advanced DNA sequencing methods should be performed in cases of C1-INH-HAE where standard approaches fail to uncover the genetic alteration.

Published
2020
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3. Validity, reliability, and responsiveness of daily monitoring visual analog scales in MASK‐air®

Author

Bernardo Sousa‐Pinto, Patrik Eklund, Oliver Pfaar, Ludger Klimek, Torsten Zuberbier, Wienczyslawa Czarlewski, Annabelle Bédard, Carsten Bindslev‐Jensen, Anna Bedbrook, Sinthia Bosnic‐Anticevich, Luisa Brussino, Victoria Cardona, Alvaro A. Cruz, Govert deVries, Philippe Devillier, Wytske J. Fokkens, José Miguel Fuentes‐Pérez, Bilun Gemicioğlu, Tari Haahtela, Yunen Rocío Huerta‐Villalobos, Juan Carlos Ivancevich, Inger Kull, Piotr Kuna, Violeta Kvedariene, Désirée E. Larenas Linnemann, Daniel Laune, Michael Makris, Erik Melén, Mário Morais‐Almeida, Ralph Mösges, Joaquim Mullol, Robyn E. O'Hehir, Nikolaos G. Papadopoulos, Ana Margarida Pereira, Emmanuel P. Prokopakis, Fotis Psarros, Frederico S. Regateiro, Sietze Reitsma, Boleslaw Samolinski, Nicola Scichilone, Jane daSilva, Cristiana Stellato, Ana Todo‐Bom, Peter Valentin Tomazic, Sanna Toppila Salmi, Antonio Valero, Arunas Valiulis, Erkka Valovirta, Michiel vanEerd, Maria Teresa Ventura, Arzu Yorgancioglu, Xavier Basagaña, Josep M. Antó, Jean Bousquet, and João Almeida Fonseca

Subjects
allergic rhinitis, mobile health, reliability, responsiveness, visual analog scales, Immunologic diseases. Allergy, RC581-607
Abstract

Abstract Background MASK‐air® is an app that supports allergic rhinitis patients in disease control. Users register daily allergy symptoms and their impact on activities using visual analog scales (VASs). We aimed to assess the concurrent validity, reliability, and responsiveness of these daily VASs. Methods Daily monitoring VAS data were assessed in MASK‐air® users with allergic rhinitis. Concurrent validity was assessed by correlating daily VAS values with those of the EuroQol‐5 Dimensions (EQ‐5D) VAS, the Control of Allergic Rhinitis and Asthma Test (CARAT) score, and the Work Productivity and Activity Impairment Allergic Specific (WPAI‐AS) Questionnaire (work and activity impairment scores). Intra‐rater reliability was assessed in users providing multiple daily VASs within the same day. Test–retest reliability was tested in clinically stable users, as defined by the EQ‐5D VAS, CARAT, or “VAS Work” (i.e., VAS assessing the impact of allergy on work). Responsiveness was determined in users with two consecutive measurements of EQ‐5D‐VAS or “VAS Work” indicating clinical change. Results A total of 17,780 MASK‐air® users, with 317,176 VAS days, were assessed. Concurrent validity was moderate–high (Spearman correlation coefficient range: 0.437–0.716). Intra‐rater reliability intraclass correlation coefficients (ICCs) ranged between 0.870 (VAS assessing global allergy symptoms) and 0.937 (VAS assessing allergy symptoms on sleep). Test–retest reliability ICCs ranged between 0.604 and 0.878—“VAS Work” and “VAS asthma” presented the highest ICCs. Moderate/large responsiveness effect sizes were observed—the sleep VAS was associated with lower responsiveness, while the global allergy symptoms VAS demonstrated higher responsiveness. Conclusion In MASK‐air®, daily monitoring VASs have high intra‐rater reliability and moderate–high validity, reliability, and responsiveness, pointing to a reliable measure of symptom loads.

Published
2021
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4. Abstracts from the 10th C1-inhibitor deficiency workshop

Author

Alvin H. Schmaier, Marco Cicardi, Avner Reshef, Dumitru Moldovan, Attila Mócsai, Margarita López-Trascasa, Alberto López Lera, Nancy J. Brown, Anastasios E. Germenis, Rafael Filippelli-Silva, Diego A. Duarte, Renan P. Martin, Camila L. Veronez, Michel Bouvier, Michael Bader, Claudio M. Costa-Neto, João Bosco Pesquero, Xavier Charest-Morin, François Marceau, Georges-É. Rivard, Arnaud Bonnefoy, Éric Wagner, Márta L. Debreczeni, Zsuzsanna Németh, Erika Kajdácsi, Endre Schwaner, László Cervenak, Gábor Oroszlán, András Szilágyi, Ráhel Dani, Péter Závodszky, Péter Gál, József Dobó, Jacques Hébert, Matthieu Vincent, Jean-Nicolas Boursiquot, Hugo Chapdeleine, Marylin Desjardins, Benoit Laramée, Rémi Gagnon, Nancy Payette, Oleksandra Lepeshkina, Delphine Charignon, Arije Ghannam, Denise Ponard, Christian Drouet, Kusumam Joseph, Baby G. Tholanikunnel, Daniel J. Sexton, Allen P. Kaplan, Stefania Loffredo, Maria Bova, Anne Lise Ferrara, Angelica Petraroli, Chiara Suffritti, Nóra Veszeli, Andrea Zanichelli, Henriette Farkas, Gianni Marone, Samuel Luyasu, Bertrand Favier, Ludovic Martin, Kinga Viktória Kőhalmi, György Temesszentandrási, Katalin Várnai, Lilian Varga, Bruce L. Zuraw, Annette Feussner, Michael A. Tortorici, Dipti Pawaskar, Huamin Henry Li, John Anderson, Jonathan A. Bernstein, Ying Zhang, Ingo Pragst, on behalf of COMPACT investigators, Emel Aygören-Pürsün, Kraig Jacobson, Jim Christensen, Arthur Van Leerberghe, Yi Wang, Jennifer Schranz, Inmaculada Martinez-Saguer, Daniel Soteres, Urs Steiner, Vesna Grivcheva Panovska, William Rae, Werner Aberer, Aarnoud Huissoon, Anette Bygum, Markus Magerl, Jochen Graff, Hilary Longhurst, Ramón Lleonart, Lei Fang, Melanie Cornpropst, Desiree Clemons, Amanda Mathis, Phil Collis, Sylvia Dobo, William P. Sheridan, Marcus Maurer, Marc A. Riedl, Timothy Craig, Aleena Banerji, Mustafa Shennak, William Yang, Jovanna Baptista, Paula Busse, Ira Kalfus, Andrew McDonald, Shawn Qian, Anthony Roberts, Con Panousis, Tim Green, Andreas Gille, Maria Zamanakou, Gedeon Loules, Dorottya Csuka, Fotis Psarros, Faidra Parsopoulou, Matthaios Speletas, Davide Firinu, Tiziana Maria Angela De Pasquale, Alessandra Zoli, Anna Radice, Stefano Pizzimenti, Emmanouil Manoussakis, George N. Konstantinou, Valeria Bafunno, Vincenzo Montinaro, Mauro Cancian, Maurizio Margaglione, Konrad Bork, Karin Wulff, Guenther Witzke, Jochen Hardt, Laurence Bouillet, Teresa Caballero, Anete S. Grumach, Christelle Pommie, Irmgard Andresen, Carmen Escuriola Ettingshausen, Zeynep Gutowski, Karin Andritschke, Richard Linde, Noémi Andrási, Tamás Szilágyi, Iris Leibovich-Nassi, Christine Symons, John Dempster, Isabelle Boccon-Gibod, Anne Pagnier, Audrey Lehmann, Kristian B. Kreiberg, Sandra A. Nieto, Raquel Martins, Renata Martins, Alejandra Menendez, Solange O. R. Valle, Margarita Olivares, Maria E. Hernandez-Landeros, Elma Nievas, Natalia Fili, Olga M. Barrera, René Bailleau, Ana Maria Gallardo-Olivos, Masumi Grau, Julian Rodriguez-Galindo, Marlon J. O. Carabantes, Edison Zapata-Venegas, Mario Martinez Alfonso, Maria Rosario-Grauert, Manuel Ratti, Daniel Vaszquez, Dario Josviack, Luis Fernando Landivar-Salinas, Oscar M. E. Calderón-Llosa, Rolando Campilay-Sarmiento, Pablo Raby, Jose Fabiani, William R. Lumry, Henrike Feuersenger, Douglas J. Watson, Thomas Machnig, on behalf of the Investigators of the COMPACT study, Donatella Lamacchia, Adriana Hernanz, Ana Alvez, Mariana Lluncor, Maria Pedrosa, Rosario Cabañas, Nieves Prior, Patrik Nordenfelt, Mats Nilsson, Anders Lindfors, Carl-Fredrik Wahlgren, Janne Björkander, Roman Hakl, Pavel Kuklínek, Irena Krčmová, Jana Hanzlíková, Martina Vachová, Radana Zachová, Marta Sobotková, Jana Strenková, Jiří Litzman, Maria Palasopoulou, Gerasimina Tsinti, Panagiota Gianni, Maria Kompoti, Sofia Garrido, Wojciech Dyga, Anna Bogdali, Aleksander Obtułowicz, Mikolajczyk Tomasz, Ewa Czarnobilska, Krystyna Obtulowicz, Teofila Książek, Anna Koncz, Dominik Gulyás, Maria Staevska, Milos Jesenak, Katarina Hrubiskova, L. Bellizzi, A. Relan, Maddalena A. Wu, Antonio Castelli, Riccardo Colombo, Gianmarco Podda, Marta Del Medico, Emanuele Catena, Francesco Casella, Francesca Perego, Nada Afifi Afifi, Eleonora Tobaldini, Nicola Montano, for the IOS Study Group, Marta Sánchez-Jareño, Marcin Stobiecki, Krystyna Obtułowicz, Irina Guryanova, Ekaterina Polyakova, Viktar Lebedz, Andrej Salivonchik, Svetlana Aleshkevich, Mikhail Belevtsev, Melanie Nordmann-Kleiner, Susanne Trainotti, Janina Hahn, Jens Greve, Liudmyla Zabrodska, Maria L. Oliva Alonso, Rosangela P. Tórtora, Alfeu T. França, Marcia G. Ribeiro, Lisa Fu, Amin Kanani, Gina Lacuesta, Susan Waserman, Stephen Betschel, Melissa I. Espinosa, Francisco A. Contreras, Martin Hrubisko, Ludmila Vavrova, Peter Banovcin, Maryam Ayazi, Mohammad Reza Fazlollahi, Shiva Saghafi, Sajedeh Mohammadian, Susan Nabilou Deshiry, Kiana Bidad, Raheleh Shokouhi Shoormasti, Iraj Mohammadzadeh, Mohammad Hassan Bemanian, Seyed Alireza Mahdaviani, Zahra Pourpak, Anna Valerieva, Mariela Vasileva, Tsvetelina Velikova, Elena Petkova, Vasil Dimitrov, Ruggero Di Maulo, on behalf of participating centers, Raz Somech, Hava Golander, Erika J. Sifuentes, Catherine Mansard, Anne Gompel, Bernard Floccard, Claire Blanchard-Delaunay, David Launay, Olivier Fain, Alain Sobel, Stéphane Gayet, Stéphanie Amarger, Guillaume Armengol, Yann Ollivier, Ariane Zélinsky-Gurung, Pierre-Yves Jeandel, Gisèle Kanny, Brigitte Coppéré, Marie Dubrel, Fabien Pelletier, Aurélie Du Thanh, Sébastien Trouiller, Jérôme Laurent, Claire De Moreuil, Christine Audouin Pajot, Alexandre Belot, Ana Rodríguez, Dasha Roa, Alicia Prieto, Maria Luisa Baeza, Borislava Krusheva, Stephanie K. A. Almeida, Rosemeire N. Constantino-Silva, Nyla Melo, Joanna Araujo Simoes, Sandra Mitie U. Palma, Jane da Silva, Bruna F. de Azevedo, Eli Mansour, Teresa González-Quevedo, Carmen Marcos, Teófilo Lobera, Blanca Sáenz de San Pedro, Ernie Avilla, Jacquie Badiou, Karen Binkley, Rozita Borici-Mazi, Linda Howlett, Paul K. Keith, Anne Rowe, Peter Waite, Aurore Billebeau, Isabelle Boccon-Gibbod, Kristina Lis, Yael Laitman, Eitan Friedman, N. M. Gokmen, O. Gulbahar, H. Onay, Z. P. Koc, and A. Z. Sin

Subjects
Immunologic diseases. Allergy, RC581-607
Published
2017
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5. A novel deep intronic SERPING1 variant as a cause of hereditary angioedema due to C1-inhibitor deficiency

Author

Faidra Parsopoulou, Grzegorz Porebski, Anna Valerieva, Krystyna Obtułowicz, Anastasios E. Germenis, Sofia Vatsiou, Gedeon Loules, Marcus Maurer, Maria Zamanakou, Matthaios Speletas, Markus Magerl, Henriette Farkas, Dorottya Csuka, Maria Staevska, and Fotis Psarros

Subjects
lcsh:Immunologic diseases. Allergy, Genotype, Intronic mutations, Genomics, Biology, DNA sequencing, C1-inhibitor deficiency, Loss of heterozygosity, symbols.namesake, Gene Frequency, Humans, Immunology and Allergy, Coding region, Genetic Predisposition to Disease, Allele, Alleles, Genetics, Sanger sequencing, Hereditary angioedema, Angioedemas, Hereditary, intronic mutations, Computational Biology, High-Throughput Nucleotide Sequencing, General Medicine, Introns, hereditary angioedema, Minor allele frequency, Mutation, Mutation (genetic algorithm), symbols, Next-generation sequencing, SERPING1 gene, next-generation sequencing, lcsh:RC581-607, Complement C1 Inhibitor Protein
Abstract

Background In about 5% of patients with hereditary angioedema due to C1-inhibitor deficiency (C1-INH-HAE) no mutation in the SERPING1 gene is detected. Methods C1-INH-HAE cases with no mutation in the coding region of SERPING1 after conventional genotyping were examined for defects in the intronic or untranslated regions of the gene. Using a next-generation sequencing (NGS) platform targeting the entire SERPING1, 14 unrelated C1-INH-HAE patients with no detectable mutations in the coding region of the gene were sequenced. Detected variants with a global minor allele frequency lower than the frequency of C1-INH-HAE (0.002%), were submitted to in silico analysis using ten different bioinformatics tools. Pedigree analysis and examination of their pathogenic effect on the RNA level were performed for filtered in variants. Results In two unrelated patients, the novel mutation c.-22-155G > T was detected in intron 1 of the SERPING1 gene by the use NGS and confirmed by Sanger sequencing. All bioinformatics tools predicted that the variant causes a deleterious effect on the gene and pedigree analysis showed its co-segregation with the disease. Degradation of the mutated allele was demonstrated by the loss of heterozygosity on the cDNA level. According to the American College of Medical Genetics and Genomics 2015 guidelines the c.-22-155G > T was curated as pathogenic. Conclusions For the first time, a deep intronic mutation that was detected by NGS in the SERPING1 gene, was proven pathogenic for C1-INH-HAE. Therefore, advanced DNA sequencing methods should be performed in cases of C1-INH-HAE where standard approaches fail to uncover the genetic alteration.

Published
2020

6. Genetic Determinants of C1 Inhibitor Deficiency Angioedema Age of Onset

Author

Henriette Farkas, Dorottya Csuka, Anastasios E. Germenis, Fotis Psarros, Markus Magerl, Gedeon Loules, Marcus Maurer, Maria Zamanakou, Matthaios Speletas, Panagiota Gianni, Maria Kompoti, and Dimitru Moldovan

Subjects
Adult, 0301 basic medicine, Adolescent, Genotype, Immunology, Bradykinin, Disease, Polymorphism, Single Nucleotide, Pathogenesis, Young Adult, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, medicine, Humans, Immunology and Allergy, Genetic Predisposition to Disease, Age of Onset, Angioedema, Allele, Child, Genetic Association Studies, Aged, Aged, 80 and over, business.industry, Angioedemas, Hereditary, Infant, General Medicine, Kallikrein, Middle Aged, Prognosis, medicine.disease, Europe, 030104 developmental biology, 030228 respiratory system, chemistry, Child, Preschool, Hereditary angioedema, Kallikreins, medicine.symptom, Age of onset, business, Biomarkers
Abstract

Background: In view of the large heterogeneity in the clinical presentation of hereditary angioedema due to C1 inhibitor deficiency (C1-INH-HAE), great efforts are being made towards detecting measurable biological determinants of disease severity that can help to improve the management of the disease. Considering the central role that plasma kallikrein plays in bradykinin production, we investigated the contribution of the functional polymorphism KLKB1-428G/A to the disease phenotype. Methods: We studied 249 C1-INH-HAE patients from 114 European families, and we explored possible associations of C1-INH-HAE clinical features with carriage of KLKB1-428G/A, combined or not with that of the functional F12-46C/T polymorphism. Results: Carriers of the G allele of the KLKB1-428G/A polymorphism exhibited a significantly delayed disease onset (i.e., by 4.1 years [p < 0.001], depending on the zygocity status), while carriers of both the KLKB1-428G/A and the F12-46C/T polymorphism displayed an 8.8-year delay in disease onset (p < 0.001) and a 64% lower probability of needing long-term prophylactic treatment (p = 0.019). Conclusions: These findings support our initial hypothesis that functional alterations in genes of proteins involved in bradykinin metabolism and function affect the clinical phenotype and possibly contribute to the pathogenesis of C1-INH-HAE. Given that an earlier onset of symptoms is inversely correlated with the subsequent course of the disease and, eventually, the need for long-term prophylaxis, these polymorphisms may be helpful prognostic biomarkers of disease severity.

Published
2017
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7. F12-46C/T polymorphism as modifier of the clinical phenotype of hereditary angioedema

Author

Matthaios Speletas, Nick Koutsostathis, Henriette Farkas, Dumitru Moldovan, Dorottya Csuka, Markus Magerl, Marcus Maurer, Ágnes Szilágyi, Anastasios E. Germenis, Maria Kompoti, Fotis Psarros, and Lilian Varga

Subjects
Adult, Male, medicine.medical_specialty, Adolescent, Genotype, DNA Mutational Analysis, Immunology, Bradykinin, Disease, Complement C1 Inactivator Proteins, Polymerase Chain Reaction, Polymorphism, Single Nucleotide, Gastroenterology, Gee, Young Adult, chemistry.chemical_compound, Internal medicine, Linear regression, Humans, Immunology and Allergy, Medicine, Child, Generalized estimating equation, Genetic Association Studies, Aged, Genetics, Factor XII, Hereditary Angioedema Types I and II, business.industry, Infant, Middle Aged, medicine.disease, Phenotype, chemistry, Child, Preschool, Mutation, Hereditary angioedema, Cohort, Female, business, Complement C1 Inhibitor Protein, Polymorphism, Restriction Fragment Length
Abstract

The factors influencing the heterogeneous clinical manifestation of hereditary angioedema due to C1-INH deficiency (C1-INH-HAE) represent one of the oldest unsolved problems of the disease. Considering that factor XII (FXII) levels may affect bradykinin production, we investigated the contribution of the functional promoter polymorphism F12-46C/T in disease phenotype. We studied 258 C1-INH-HAE patients from 113 European families, and we explored possible associations of F12-46C/T with clinical features and the SERPING1 mutational status. Given that our cohort consisted of related subjects, we implemented generalized estimating equations (GEEs), an extension of the generalized linear model accounting for the within-subject correlation. F12-46C/T carriers exhibited a significantly delayed disease onset (P

Published
2015
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8. Contents Vol. 164, 2014

Author

Rosemary Walsh, Luca Reggiani Bonetti, Ali H. Ziyab, Petra Šimůnková, Nick Koutsostathis, Yesim Kaymak, Asuman Karakaya, Simona Partlová, Fotis Psarros, Elisa Montaldo, Mahmut Dogru, Arnold S. Kirshenbaum, Evangelia Farmaki, Syed Hasan Arshad, Ozge Cemiloglu Ulker, Maria Cristina Mingari, Lorenzo Moretta, Wilfried Karmaus, Satz Mengensatzproduktion, John W. Holloway, Hongmei Zhang, J. Uhlík, Dean D. Metcalfe, Francesca Moretta, Rahime Gul Yesiltepe Mutlu, Susan E. Steck, Thomas Ried, Amy Petrik, Susan Ewart, Franco Locatelli, Seda Ozturkmen, Heves Kirmizibekmez, Paola Vacca, Pietro Merli, Druckerei Stückle, Jiří Jarkovský, Sury Vepa, Anastasios E. Germenis, Juan A Rivera, Marie Žaloudíková, L. Vajner, Matthaios Speletas, Cristian Palmiere, Ryo Suzuki, Danny Wangsa, Alev Aktas, Tara L. Kirby, Barbara Dema, and Genny Del Zotto

Subjects
business.industry, Immunology, Immunology and Allergy, Medicine, General Medicine, business
Published
2014
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9. Modulation of the epithelial inflammatory response to rhinovirus in an atopic environment

Author

Photini Saxoni-Papageorgiou, Mina Gaga, Fotis Psarros, Nikolaos G. Papadopoulos, M. Xatzipsalti, George N. Konstantinou, and Dimitrios Gourgiotis

Subjects
Adult, Hypersensitivity, Immediate, Male, Allergy, Rhinovirus, Immunology, Bronchi, Inflammation, Biology, Virus Replication, medicine.disease_cause, Peripheral blood mononuclear cell, Monocytes, Transforming Growth Factor beta1, Interferon-gamma, Immune system, Immunopathology, medicine, Humans, Immunology and Allergy, Respiratory system, Bronchitis, Cells, Cultured, Picornaviridae Infections, Cell Death, Epithelial Cells, medicine.disease, Asthma, Up-Regulation, Culture Media, Conditioned, Antibody Formation, Cytokines, Respiratory epithelium, Female, Inflammation Mediators, medicine.symptom
Abstract

Background Immune responses to rhinovirus (RV) as well as direct effects of RV on respiratory epithelium may contribute to the induction of asthma exacerbations. Objective To evaluate the effect of the environment resulting from an atopic immune response on RV-induced epithelial inflammation, replication and cytotoxicity. Methods Peripheral blood mononuclear cells (PBMC) from atopic asthmatic subjects and matched controls (12 pairs) were isolated and stimulated by RVs. Human bronchial epithelial (BEAS-2B) cells were infected with RV in the presence of conditioned media from RV-stimulated PBMC cultures. IL-6, IL-8, RANTES and TGF-beta1 levels were measured by ELISA, RV-induced cytotoxicity by a colorimetric method and RV titres on Ohio-HeLa cells. Results RV-induced epithelial production of IL-6, IL-8 and RANTES was significantly lower, while TGF-beta1 was higher when cells were exposed to conditioned media from atopic asthmatic subjects compared with those from normal controls. Exposure to the 'atopic' environment also resulted in elevated RV titres and increased RV-induced cytotoxicity. Conclusions Under the influence of an atopic environment, the epithelial inflammatory response to RV is down-regulated, associated with increased viral proliferation and augmented cell damage, while TGF is up-regulated. These changes may help explain the propensity of atopic asthmatic individuals to develop lower airway symptoms after respiratory infections and indicate a mechanism through which viral infections may promote airway remodelling.

Published
2008
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10. The Rate of Atopy in Patients with Cold-Induced Urticaria

Author

Ekaterini Syrigou, Fotis Psarros, Nikolaos Syrigos, and Marianna Tziotou

Subjects
Atopy, medicine.medical_specialty, business.industry, Immunology, Immunology and Allergy, Medicine, Cold-induced urticaria, In patient, business, medicine.disease, Dermatology
Published
2017
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