TY - JOUR A1 - Bousquet, J. A1 - Anto, J. M. A1 - Akdis, M. A1 - Auffray, C. A1 - Keil, T. A1 - Momas, I. A1 - Postma, D. S. A1 - Valenta, R. A1 - Wickman, M. A1 - Cambon-Thomsen, A. A1 - Haahtela, T. A1 - Lambrecht, B. N. A1 - Lodrup Carlsen, K. C. A1 - Koppelman, G. H. A1 - Sunyer, J. A1 - Zuberbier, T. A1 - Annesi-Maesano, I. A1 - Arno, A. A1 - Bindslev-Jensen, C. A1 - De Carlo, G. A1 - Forastiere, F. A1 - Heinrich, J. A1 - Kowalski, M. L. A1 - Maier, D. A1 - Melen, E. A1 - Palkonen, S. A1 - Smit, H. A. A1 - Standl, M. A1 - Wright, J. A1 - Asarnoj, A. A1 - Benet, M. A1 - Ballardini, N. A1 - Garcia-Aymerich, J. A1 - Gehring, U. A1 - Guerra, S. A1 - Hohman, C. A1 - Kull, I. A1 - Lupinek, C. A1 - Pinart, M. A1 - Skrindo, I. A1 - Westman, M. A1 - Smagghe, D. A1 - Akdis, C. A1 - Albang, R. A1 - Anastasova, V. A1 - Anderson, N. A1 - Bachert, C. A1 - Ballereau, S. A1 - Ballester, F. A1 - Basagana, X. A1 - Bedbrook, A. A1 - Bergstrom, A. A1 - von Berg, A. A1 - Brunekreef, B. A1 - Burte, E. A1 - Carlsen, K.H. A1 - Chatzi, L. A1 - Coquet, J.M. A1 - Curin, M. A1 - Demoly, P. A1 - Eller, E. A1 - Fantini, M.P. A1 - Gerhard, B. A1 - Hammad, H. A1 - von Hertzen, L. A1 - Hovland, V. A1 - Jacquemin, B. A1 - Just, J. A1 - Keller, T. A1 - Kerkhof, M. A1 - Kiss, R. A1 - Kogevinas, M. A1 - Koletzko, S. A1 - Lau, S. A1 - Lehmann, I. A1 - Lemonnier, N. A1 - McEachan, R. A1 - Makela, M. A1 - Mestres, J. A1 - Minina, E. A1 - Mowinckel, P. A1 - Nadif, R. A1 - Nawijn, M. A1 - Oddie, S. A1 - Pellet, J. A1 - Pin, I. A1 - Porta, D. A1 - Rancière, F. A1 - Rial-Sebbag, A. A1 - Schuijs, M.J. A1 - Siroux, V. A1 - Tischer, C.G. A1 - Torrent, M. A1 - Varraso, R. A1 - De Vocht, J. A1 - Wenger, K. A1 - Wieser, S. A1 - Xu, C. T1 - Paving the way of systems biology and precision medicine in allergic diseases: the MeDALL success story Mechanisms of the Development of ALLergy; EUFP7-CP-IP; Project No: 261357; 2010-2015 JF - Allergy N2 - MeDALL (Mechanisms of the Development of ALLergy; EU FP7-CP-IP; Project No: 261357; 2010-2015) has proposed an innovative approach to develop early indicators for the prediction, diagnosis, prevention and targets for therapy. MeDALL has linked epidemiological, clinical and basic research using a stepwise, large-scale and integrative approach: MeDALL data of precisely phenotyped children followed in 14 birth cohorts spread across Europe were combined with systems biology (omics, IgE measurement using microarrays) and environmental data. Multimorbidity in the same child is more common than expected by chance alone, suggesting that these diseases share causal mechanisms irrespective of IgE sensitization. IgE sensitization should be considered differently in monosensitized and polysensitized individuals. Allergic multimorbidities and IgE polysensitization are often associated with the persistence or severity of allergic diseases. Environmental exposures are relevant for the development of allergy-related diseases. To complement the population-based studies in children, MeDALL included mechanistic experimental animal studies and in vitro studies in humans. The integration of multimorbidities and polysensitization has resulted in a new classification framework of allergic diseases that could help to improve the understanding of genetic and epigenetic mechanisms of allergy as well as to better manage allergic diseases. Ethics and gender were considered. MeDALL has deployed translational activities within the EU agenda. KW - asthma KW - birth cohort KW - atopic-dermatitis KW - immune-responses KW - IgE KW - multimorbidity KW - polysensitization KW - rhinitis KW - chronic respiratory-diseases KW - childhood asthma KW - immunological reactivity KW - IgE sensitazion KW - immunoglobulin-e KW - integraed care Y1 - 2016 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-186858 VL - 71 IS - 11 ER - TY - JOUR A1 - Bousquet, Jean A1 - Anto, Josep M. A1 - Bachert, Claus A1 - Haahtela, Tari A1 - Zuberbier, Torsten A1 - Czarlewski, Wienczyslawa A1 - Bedbrook, Anna A1 - Bosnic‐Anticevich, Sinthia A1 - Walter Canonica, G. A1 - Cardona, Victoria A1 - Costa, Elisio A1 - Cruz, Alvaro A. A1 - Erhola, Marina A1 - Fokkens, Wytske J. A1 - Fonseca, Joao A. A1 - Illario, Maddalena A1 - Ivancevich, Juan‐Carlos A1 - Jutel, Marek A1 - Klimek, Ludger A1 - Kuna, Piotr A1 - Kvedariene, Violeta A1 - Le, LTT A1 - Larenas‐Linnemann, Désirée E. A1 - Laune, Daniel A1 - Lourenço, Olga M. A1 - Melén, Erik A1 - Mullol, Joaquim A1 - Niedoszytko, Marek A1 - Odemyr, Mikaëla A1 - Okamoto, Yoshitaka A1 - Papadopoulos, Nikos G. A1 - Patella, Vincenzo A1 - Pfaar, Oliver A1 - Pham‐Thi, Nhân A1 - Rolland, Christine A1 - Samolinski, Boleslaw A1 - Sheikh, Aziz A1 - Sofiev, Mikhail A1 - Suppli Ulrik, Charlotte A1 - Todo‐Bom, Ana A1 - Tomazic, Peter‐Valentin A1 - Toppila‐Salmi, Sanna A1 - Tsiligianni, Ioanna A1 - Valiulis, Arunas A1 - Valovirta, Erkka A1 - Ventura, Maria‐Teresa A1 - Walker, Samantha A1 - Williams, Sian A1 - Yorgancioglu, Arzu A1 - Agache, Ioana A1 - Akdis, Cezmi A. A1 - Almeida, Rute A1 - Ansotegui, Ignacio J. A1 - Annesi‐Maesano, Isabella A1 - Arnavielhe, Sylvie A1 - Basagaña, Xavier A1 - D. Bateman, Eric A1 - Bédard, Annabelle A1 - Bedolla‐Barajas, Martin A1 - Becker, Sven A1 - Bennoor, Kazi S. A1 - Benveniste, Samuel A1 - Bergmann, Karl C. A1 - Bewick, Michael A1 - Bialek, Slawomir A1 - E. Billo, Nils A1 - Bindslev‐Jensen, Carsten A1 - Bjermer, Leif A1 - Blain, Hubert A1 - Bonini, Matteo A1 - Bonniaud, Philippe A1 - Bosse, Isabelle A1 - Bouchard, Jacques A1 - Boulet, Louis‐Philippe A1 - Bourret, Rodolphe A1 - Boussery, Koen A1 - Braido, Fluvio A1 - Briedis, Vitalis A1 - Briggs, Andrew A1 - Brightling, Christopher E. A1 - Brozek, Jan A1 - Brusselle, Guy A1 - Brussino, Luisa A1 - Buhl, Roland A1 - Buonaiuto, Roland A1 - Calderon, Moises A. A1 - Camargos, Paulo A1 - Camuzat, Thierry A1 - Caraballo, Luis A1 - Carriazo, Ana‐Maria A1 - Carr, Warner A1 - Cartier, Christine A1 - Casale, Thomas A1 - Cecchi, Lorenzo A1 - Cepeda Sarabia, Alfonso M. A1 - H. Chavannes, Niels A1 - Chkhartishvili, Ekaterine A1 - Chu, Derek K. A1 - Cingi, Cemal A1 - Correia de Sousa, Jaime A1 - Costa, David J. A1 - Courbis, Anne‐Lise A1 - Custovic, Adnan A1 - Cvetkosvki, Biljana A1 - D'Amato, Gennaro A1 - da Silva, Jane A1 - Dantas, Carina A1 - Dokic, Dejan A1 - Dauvilliers, Yves A1 - De Feo, Giulia A1 - De Vries, Govert A1 - Devillier, Philippe A1 - Di Capua, Stefania A1 - Dray, Gerard A1 - Dubakiene, Ruta A1 - Durham, Stephen R. A1 - Dykewicz, Mark A1 - Ebisawa, Motohiro A1 - Gaga, Mina A1 - El‐Gamal, Yehia A1 - Heffler, Enrico A1 - Emuzyte, Regina A1 - Farrell, John A1 - Fauquert, Jean‐Luc A1 - Fiocchi, Alessandro A1 - Fink‐Wagner, Antje A1 - Fontaine, Jean‐François A1 - Fuentes Perez, José M. A1 - Gemicioğlu, Bilun A1 - Gamkrelidze, Amiran A1 - Garcia‐Aymerich, Judith A1 - Gevaert, Philippe A1 - Gomez, René Maximiliano A1 - González Diaz, Sandra A1 - Gotua, Maia A1 - Guldemond, Nick A. A1 - Guzmán, Maria‐Antonieta A1 - Hajjam, Jawad A1 - Huerta Villalobos, Yunuen R. A1 - Humbert, Marc A1 - Iaccarino, Guido A1 - Ierodiakonou, Despo A1 - Iinuma, Tomohisa A1 - Jassem, Ewa A1 - Joos, Guy A1 - Jung, Ki‐Suck A1 - Kaidashev, Igor A1 - Kalayci, Omer A1 - Kardas, Przemyslaw A1 - Keil, Thomas A1 - Khaitov, Musa A1 - Khaltaev, Nikolai A1 - Kleine‐Tebbe, Jorg A1 - Kouznetsov, Rostislav A1 - Kowalski, Marek L. A1 - Kritikos, Vicky A1 - Kull, Inger A1 - La Grutta, Stefania A1 - Leonardini, Lisa A1 - Ljungberg, Henrik A1 - Lieberman, Philip A1 - Lipworth, Brian A1 - Lodrup Carlsen, Karin C. A1 - Lopes‐Pereira, Catarina A1 - Loureiro, Claudia C. A1 - Louis, Renaud A1 - Mair, Alpana A1 - Mahboub, Bassam A1 - Makris, Michaël A1 - Malva, Joao A1 - Manning, Patrick A1 - Marshall, Gailen D. A1 - Masjedi, Mohamed R. A1 - Maspero, Jorge F. A1 - Carreiro‐Martins, Pedro A1 - Makela, Mika A1 - Mathieu‐Dupas, Eve A1 - Maurer, Marcus A1 - De Manuel Keenoy, Esteban A1 - Melo‐Gomes, Elisabete A1 - Meltzer, Eli O. A1 - Menditto, Enrica A1 - Mercier, Jacques A1 - Micheli, Yann A1 - Miculinic, Neven A1 - Mihaltan, Florin A1 - Milenkovic, Branislava A1 - Mitsias, Dimitirios I. A1 - Moda, Giuliana A1 - Mogica‐Martinez, Maria‐Dolores A1 - Mohammad, Yousser A1 - Montefort, Steve A1 - Monti, Ricardo A1 - Morais‐Almeida, Mario A1 - Mösges, Ralph A1 - Münter, Lars A1 - Muraro, Antonella A1 - Murray, Ruth A1 - Naclerio, Robert A1 - Napoli, Luigi A1 - Namazova‐Baranova, Leyla A1 - Neffen, Hugo A1 - Nekam, Kristoff A1 - Neou, Angelo A1 - Nordlund, Björn A1 - Novellino, Ettore A1 - Nyembue, Dieudonné A1 - O'Hehir, Robyn A1 - Ohta, Ken A1 - Okubo, Kimi A1 - Onorato, Gabrielle L. A1 - Orlando, Valentina A1 - Ouedraogo, Solange A1 - Palamarchuk, Julia A1 - Pali‐Schöll, Isabella A1 - Panzner, Peter A1 - Park, Hae‐Sim A1 - Passalacqua, Gianni A1 - Pépin, Jean‐Louis A1 - Paulino, Ema A1 - Pawankar, Ruby A1 - Phillips, Jim A1 - Picard, Robert A1 - Pinnock, Hilary A1 - Plavec, Davor A1 - Popov, Todor A. A1 - Portejoie, Fabienne A1 - Price, David A1 - Prokopakis, Emmanuel P. A1 - Psarros, Fotis A1 - Pugin, Benoit A1 - Puggioni, Francesca A1 - Quinones‐Delgado, Pablo A1 - Raciborski, Filip A1 - Rajabian‐Söderlund, Rojin A1 - Regateiro, Frederico S. A1 - Reitsma, Sietze A1 - Rivero‐Yeverino, Daniela A1 - Roberts, Graham A1 - Roche, Nicolas A1 - Rodriguez‐Zagal, Erendira A1 - Rolland, Christine A1 - Roller‐Wirnsberger, Regina E. A1 - Rosario, Nelson A1 - Romano, Antonino A1 - Rottem, Menachem A1 - Ryan, Dermot A1 - Salimäki, Johanna A1 - Sanchez‐Borges, Mario M. A1 - Sastre, Joaquin A1 - Scadding, Glenis K. A1 - Scheire, Sophie A1 - Schmid‐Grendelmeier, Peter A1 - Schünemann, Holger J. A1 - Sarquis Serpa, Faradiba A1 - Shamji, Mohamed A1 - Sisul, Juan‐Carlos A1 - Sofiev, Mikhail A1 - Solé, Dirceu A1 - Somekh, David A1 - Sooronbaev, Talant A1 - Sova, Milan A1 - Spertini, François A1 - Spranger, Otto A1 - Stellato, Cristiana A1 - Stelmach, Rafael A1 - Thibaudon, Michel A1 - To, Teresa A1 - Toumi, Mondher A1 - Usmani, Omar A1 - Valero, Antonio A. A1 - Valenta, Rudolph A1 - Valentin‐Rostan, Marylin A1 - Pereira, Marilyn Urrutia A1 - van der Kleij, Rianne A1 - Van Eerd, Michiel A1 - Vandenplas, Olivier A1 - Vasankari, Tuula A1 - Vaz Carneiro, Antonio A1 - Vezzani, Giorgio A1 - Viart, Frédéric A1 - Viegi, Giovanni A1 - Wallace, Dana A1 - Wagenmann, Martin A1 - Wang, De Yun A1 - Waserman, Susan A1 - Wickman, Magnus A1 - Williams, Dennis M. A1 - Wong, Gary A1 - Wroczynski, Piotr A1 - Yiallouros, Panayiotis K. A1 - Yusuf, Osman M. A1 - Zar, Heather J. A1 - Zeng, Stéphane A1 - Zernotti, Mario E. A1 - Zhang, Luo A1 - Shan Zhong, Nan A1 - Zidarn, Mihaela T1 - ARIA digital anamorphosis: Digital transformation of health and care in airway diseases from research to practice JF - Allergy N2 - Digital anamorphosis is used to define a distorted image of health and care that may be viewed correctly using digital tools and strategies. MASK digital anamorphosis represents the process used by MASK to develop the digital transformation of health and care in rhinitis. It strengthens the ARIA change management strategy in the prevention and management of airway disease. The MASK strategy is based on validated digital tools. Using the MASK digital tool and the CARAT online enhanced clinical framework, solutions for practical steps of digital enhancement of care are proposed. KW - ARIA KW - asthma KW - CARAT KW - digital transformation of health and care KW - MASK KW - rhinitis Y1 - 2021 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-228339 VL - 76 IS - 1 SP - 168 EP - 190 ER - TY - JOUR A1 - Forchert, Leandra A1 - Potapova, Ekaterina A1 - Panetta, Valentina A1 - Dramburg, Stephanie A1 - Perna, Serena A1 - Posa, Daniela A1 - Resch‐Marat, Yvonne A1 - Lupinek, Christian A1 - Rohrbach, Alexander A1 - Grabenhenrich, Linus A1 - Icke, Katja A1 - Bauer, Carl‐Peter A1 - Hoffman, Ute A1 - Forster, Johannes A1 - Zepp, Fred A1 - Schuster, Antje A1 - Wahn, Ulrich A1 - Keil, Thomas A1 - Lau, Susanne A1 - Vrtala, Susanne A1 - Valenta, Rudolf A1 - Matricardi, Paolo Maria T1 - Der p 23‐specific IgE response throughout childhood and its association with allergic disease: A birth cohort study JF - Pediatric Allergy and Immunology N2 - Background The Dermatophagoides pteronyssinus molecule Der p 23 is a major allergen whose clinical relevance has been shown in cross‐sectional studies. We longitudinally analysed the trajectory of Der p 23‐specific IgE antibody (sIgE) levels throughout childhood and youth, their early‐life determinants and their clinical relevance for allergic rhinitis and asthma. Methods We obtained sera and clinical data of 191 participants of the German Multicentre Allergy Study, a prospective birth cohort. Serum samples from birth to 20 years of age with sIgE reactivity to Der p 23 in a customised semiquantitative microarray were newly analysed with a singleplex quantitative assay. Early mite exposure was assessed by measuring the average content of Der p 1 in house dust at 6 and 18 months. Results Der p 23‐sIgE levels were detected at least once in 97/191 participants (51%). Prevalence of Der p 23 sensitisation and mean sIgE levels increased until age 10 years, plateaued until age 13 years and were lowest at age 20 years. Asthma, allergic rhinitis (AR) and atopic dermatitis (AD) were more prevalent in Der p 23‐sensitised children, including those with monomolecular but persistent sensitisation (11/97, 11%). A higher exposure to mites in infancy and occurrence of AD before 5 years of age preceded the onset of Der p 23 sensitisation, which in turn preceded a higher incidence of asthma. Conclusions Der p 23 sensitisation peaks in late childhood and then decreases. It is preceded by early mite exposure and AD. Asthma and AR can occur in patients persistently sensitised to Der p 23 as the only mite allergen, suggesting the inclusion of molecular testing of Der p 23‐sIgE for subjects with clinical suspicion of HDM allergy but without sIgE to other major D.pt. allergens. KW - asthma KW - birth cohort KW - childhood KW - Der p 23 KW - house dust mite allergy KW - IgE Y1 - 2022 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-287181 VL - 33 IS - 7 ER - TY - THES A1 - Gogishvili, Tea T1 - Immunotherapy of allergic disorders in a mouse model of allergic airway inflammation T1 - Immuntherapie allergischer Erkrankungen in einem Mausmodell für allergische Atemwegsentzündungen N2 - Allergische Erkrankungen sind Störungen, bei denen es zu Immunfehlregulationen kommt und die bei empfänglichen Individuen zur Entstehung von Allergen spezifischen T-Helfer 2 (TH2) Immunantworten führen. Neuere Untersuchungen deuten darauf hin, dass die für Soforttypallergien charakteristischen TH2 Immunantworten sowohl durch natürlich vorkommende CD4+CD25+ regulatorische T Zellen (Treg) als auch durch Antigen induzierte IL-10-secreting CD4+ regulatorische T Zellen kontrolliert werden können. Weiterhin gibt es Hinweise, dass eine erfolgreiche Allergen spezifische Immuntherapie über die Induktion von IL-10 sezernierenden T reg Zellen vermittelt wird. In ersten Teil der Arbeit wird die Effizienz einer Allergen spezifischen Immuntherapie (SIT) in einem Mausmodel für allergische Atemwegsentzündung demonstriert. Als Allergieparameter wurden Allergen spezifisches IgE im Serum, verschiedene TH1 und TH2 Cytokine in der brochoalveolären Lavage Flüssigkeit und nach in vitro Restimulation in Milzzellen untersucht. Weiterhin wurden Histologien von Lungengewebe angefertigt, um das eosinophile Entzündungsinfiltrat und die Asthma typische Becherzellmetaplasie darzustellen. Weiterhin wurden durch FACS Untersuchungen regulatorische T Zellen nachgewiesen. Es konnte gezeigt werden, dass im Mausmodell die intranasale Applikationsform der SIT die allergischen Symptome effizienter bekämpfen konnte, als die beim Menschen etablierte subcutane Applikationsform. Um Mechanismen zu definieren die eine SIT effizienter machen könnten wurde ein IL-4/IL13 Inhibitor (QY) als Adjuvans für die SIT benutzt. Für den Zytokininhibitor konnte gezeigt werden, dass bei einer Applikation während der allergischen Sensibilisierung die Entstehung einer TH2 Immunantwort und die Ausbildung allergischer Symptome verhindert wird. Die Applikation des Inhibitors zusammen mit einer SIT zeigte jedoch keine zusätzlichen signifikanten antiallergischen Effekte im Vergleich zur Durchführung der SIT als Monotherapie. Diese Ergebnisse deuten möglicherweise daraufhin , dass der bekannte Wechsel einer TH2 Immunantwort zu einer TH1 Antwort während der SIT nicht der Schlüsselmechanismus zu einer erfolgreichen Behandlung ist. Insbesondere weil unter der SIT auch in unserem Mausmodell die Induktion von IL-10 sezernierenden CD4+ T regulatorischen Zellen mit der Suppression der allergischen Atemwegsentzüdnung vergesellschaftet waren, so dass möglicherwiese diese Zellen für den Therapieerfolg relevant sind . Um die Rolle regulatorischer T Zellen im Allergiemodell näher zu beleuchten wurde im 2. Teil der Arbeit ein monoklonaler superagonistischer anti-CD28 Antikörper benutzt, von dem bekannt ist dass T regulatorische Zellen in vivo induziert werden. Es konnte gezeigt werden, dass die Applikation des Antikörpers während der allergischen Sensibilisierung die Etablierung einer TH2 Immunantwort verstärkte. Im Gegensatz dazu wurden durch die therapeutische Applikation des anti CD28 Antikörpers in einer etablierten Allergie, IL-10 sezernierende CD4+CD25+ T Zellen induziert, welches mit einer Abschwächung der gemessenen Allergieparameter einherging. N2 - Allergic disease are inflammatory disorders in which aberrant immune regulation occurs, and susceptible individuals mount allergen specific T helper 2 (Th2) responses, which drives disease pathology. Recent studies indicate that Th2 responses that are characteristic of allergic manifestations can be regulated by both naturally occurring CD4+CD25+ regulatory (Treg) cells and antigen-driven IL-10-secreting CD4+ regulatory T cells. Evidence is also emerging that successful Allergen specific immunotherapy (SIT) might work through the induction of IL-10-secreting regulatory T cells. In the first part of this work, I demonstrated the efficiency of allergen specific immunotherapy in the mouse model for allergic airway inflammation. Here I could show that intranasal administration of SIT abrogates allergic symptoms more efficiently, than the subcutaneous treatment. Furthermore, an IL-4/IL-13 (QY) inhibitor was used as an adjuvant for SIT, which has been demonstrated to have an anti-allergic potential, when administered prophylactically during allergic sensitization. However, the combination therapy with SIT and the inhibitory molecule QY did not show any significant enhancement in regards to all measured allergic parameters, when compared to monotherapy with SIT. These results provide the evidence, that shift from Th2 to Th1 cytokine profile might not be a key event in successful SIT. Subsequently, the investigation of immune mechanisms under successful SIT demonstrate that the increase of IL-10 secreting CD4+ T regulatory cells is associated with the suppression of airway inflammation in our mouse system, suggesting that these T cell subsets might be involved in the regulatory mechanisms of allergic disorders. In agreement with these findings is the second part of this work, where superagonistic a-CD28 mAb´s were used for the expansion of T regulatory cell subsets in our murine model for allergic airway inflammation. Here I could show, that the application of a-CD28 mAb during allergic sensitization, resulted in the establishment of a Th2 state, rather than a stimulation of a Treg cell population, supporting the Th2 promoting role of a-CD28 mAb together with TCR engagement. However, interesting findings were obtained by application of the superagonistic a-CD28 mAb in the challenge phase in established allergy. Conversely to the previous experiment, therapeutic administration of a-CD28 mAb lead to the generation of IL-10 secreting CD4+CD25+ T cell population in line with the induction of anti-allergic effects. Taking together the results of this study argue for the anti-inflammatory properties of T regulatory cells in allergic disease and highlights importance of these T cell subsets in the suppression of Th2 cell-driven response to allergen. Moreover, these observations suggest that the induction of IL-10 in vivo by T regulatory cells may represent a novel treatment strategy for allergic disorders. KW - Bronchialasthma KW - Allergie KW - Maus KW - Immuntherapie KW - Allergy KW - asthma KW - IL-4/IL-13 inhibitor KW - Mouse model of allergic airway inflammation Y1 - 2006 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-19304 ER - TY - JOUR A1 - Hasenpusch, Claudia A1 - Matterne, Uwe A1 - Tischer, Christina A1 - Hrudey, Ilona A1 - Apfelbacher, Christian T1 - Development and content validation of a comprehensive health literacy survey instrument for use in individuals with asthma during the COVID-19 pandemic JF - International Journal of Environmental Research and Public Health N2 - Individuals with chronic conditions have been faced with many additional challenges during the COVID-19 pandemic. Individual health literacy (HL) as the ability to access, understand, evaluate, and apply pandemic-related information has thus become ever more important in these populations. The purpose of this study was to develop and content-validate a comprehensive HL survey instrument for people with asthma based on an integrated framework, and on previous surveys and other instruments for use in the general population and vulnerable groups. Beside HL, assumed determinants, mediators, and health outcomes were embraced in the framework. A mixed-method design was used. A comprehensive examination of the available literature yielded an initial pool of 398 single items within 20 categories. Based on content validity indices (CVI) of expert ratings (n = 11) and the content analysis of cognitive interviews with participants (n = 9), the item pool was reduced, and individual items/scales refined or modified. The instrument showed appropriate comprehensibility (98.0%), was judged relevant, and had an acceptable CVI at scale level (S-CVI/Ave = 0.91). The final version comprises 14 categories measured by 38 questions consisting of 116 single items. In terms of content, the instrument appears a valid representation of behavioural and psychosocial constructs pertaining to a broad HL understanding and relevant to individuals with asthma during the COVID-19 pandemic. Regular monitoring of these behavioural and psychosocial constructs during the course of the pandemic can help identify needs as well as changes during the course of the pandemic, which is particularly important in chronic disease populations. KW - SARS-CoV-2 KW - COVID-19 KW - asthma KW - survey instrument KW - questionnaire development KW - health literacy Y1 - 2022 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-262146 SN - 1660-4601 VL - 19 IS - 4 ER - TY - JOUR A1 - Held, Matthias A1 - Mittnacht, Maria A1 - Kolb, Martin A1 - Karl, Sabine A1 - Jany, Berthold T1 - Pulmonary and Cardiac Function in Asymptomatic Obese Subjects and Changes following a Structured Weight Reduction Program: A Prospective Observational Study JF - PLOS ONE N2 - Background The prevalence of obesity is rising. Obesity can lead to cardiovascular and ventilatory complications through multiple mechanisms. Cardiac and pulmonary function in asymptomatic subjects and the effect of structured dietary programs on cardiac and pulmonary function is unclear. Objective To determine lung and cardiac function in asymptomatic obese adults and to evaluate whether weight loss positively affects functional parameters. Methods We prospectively evaluated bodyplethysmographic and echocardiographic data in asymptomatic subjects undergoing a structured one-year weight reduction program. Results 74 subjects (32 male, 42 female; mean age 42±12 years) with an average BMI 42.5±7.9, body weight 123.7±24.9 kg were enrolled. Body weight correlated negatively with vital capacity (R = −0.42, p<0.001), FEV1 (R = −0.497, p<0.001) and positively with P 0.1 (R = 0.32, p = 0.02) and myocardial mass (R = 0.419, p = 0.002). After 4 months the study subjects had significantly reduced their body weight (−26.0±11.8 kg) and BMI (−8.9±3.8) associated with a significant improvement of lung function (absolute changes: vital capacity +5.5±7.5% pred., p<0.001; FEV1+9.8±8.3% pred., p<0.001, ITGV+16.4±16.0% pred., p<0.001, SR tot −17.4±41.5% pred., p<0.01). Moreover, P0.1/Pimax decreased to 47.7% (p<0.01) indicating a decreased respiratory load. The change of FEV1 correlated significantly with the change of body weight (R = −0.31, p = 0.03). Echocardiography demonstrated reduced myocardial wall thickness (−0.08±0.2 cm, p = 0.02) and improved left ventricular myocardial performance index (−0.16±0.35, p = 0.02). Mitral annular plane systolic excursion (+0.14, p = 0.03) and pulmonary outflow acceleration time (AT +26.65±41.3 ms, p = 0.001) increased. Conclusion Even in asymptomatic individuals obesity is associated with abnormalities in pulmonary and cardiac function and increased myocardial mass. All the abnormalities can be reversed by a weight reduction program. KW - pulmonary hypertension KW - echocardiography KW - morbid obesity KW - asthma KW - pulmonary function KW - weight loss KW - body weight KW - obesity Y1 - 2014 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-119239 VL - 9 IS - 9 ER - TY - THES A1 - Heller, Julia T1 - Rezidive bei Polyposis nasi nach operativer Therapie - ätiologische und prognostische Faktoren T1 - Recurrence rates of chronic polypoid sinusitis after surgery of the nasal sinuses - ätiologic and prognostic factors N2 - Kurzfassung in Deutsch: Trotz intensivster Forschung in den letzten Jahrzehnten, bleiben letztlich Äthiologie und Pathogenese der Polyposis nasi weitgehend ungeklärt. In der Behandlung fehlt daher ein kausaler Therapieansatz, die Therapie der Wahl besteht bislang in der chirurgischen Sanierung der betroffenen Nasennebenhöhlen. Die hohen Rezidivraten nach operativer Therapie stellen jedoch ein großes Problem dar. Die Polyposis nasi scheint eine hohe Assoziation zu zeigen mit den Begleiterkrankungen Asthma bronchiale, Aspirin- Intoleranz und Allergien. Um herauszufinden inwieweit diese den postoperativen Heilungsverlauf und die Rezidivhäufigkeit beeinflussen, wurden in dieser Arbeit 54 Patienten, die in den Jahren 1991 bis einschließlich 1993 an der Würzburger Universitätsklinik für Hals-, Nasen- und Ohrenkrankheiten aufgrund der Primärdiagnose Polyposis nasi operiert worden waren mittels der Daten aus den Krankenakten sowie eines speziell entwickelten Fragebogens über einen Zeitraum von mindestens zehn Jahren postoperativ nachbeobachtet. Neben den drei Begleiterkrankungen wurden die Risikofaktoren Nikotin- und Alkoholkonsum sowie die postoperative Verwendung topischer Kortikoide mit den Daten zu Geschlecht, Alter, postoperativen Beschwerden, der Rezidivhäufigkeit und der Gesamtzahl der Operationen pro Patient korreliert. Im untersuchten Patientengut war überwiegend das männliche Geschlecht betroffen, die Patienten zumeist mindestens dreißig Jahre alt. Innerhalb von zehn Jahren traten Rezidive bei 22% der Patienten auf. Etwa jeder 5. Polypenpatient (22%) litt unter Asthma bronchiale, 17% der Patienten unter einer Aspirin- Intoleranz. In unserer Auswertung zeigten beider Erkrankungen keinen negativen Einfluss auf die postoperative Rezidivwahrscheinlichkeit. Über die Hälfte der Patienten litten unter Allergien, bei diesen Personen traten Rezidive seltener auf, als bei den Nichtallergikern. Dieses Ergebniss unterstützt die aktuellen Thesen in der Literatur, dass Allergien keine negative Auswirkung auf die chronisch polypöse Sinusitis zeigen. Unsere Daten zur postoperativen Lokaltherapie können die Angaben aus der Literatur bestätigen, dass topisch verabreichte Kortikosteroide eine Ausheilung der Nasenpolypen begünstigen und Rezidive vermindern. Da bei einem Viertel unserer Patienten die Nasenpolypen familiär gehäuft auftraten, lässt sich eine genetische Komponente in der Pathogenese der Nasenpolypen vermuten. Unter den Alkoholkonsumenten fanden wir deutlich höhere Rezidivraten als unter den Patienten, die dies verneinten. In histologischen Arbeiten wurde bereits von einer Störung der mukoziliären Clearance der respiratorischen Schleimhaut durch Alkohol berichteten, möglicherweise könnte Alkoholgenuss über diesen Mechanismus eine Polypenbildung begünstigen. Nikotin hatte in unserer Arbeit keinen Einfluss auf die Polypenbildung. Aufgrund unserer Ergebnisse wird die Hypothese aufgestellt, dass Alkoholkonsum und hereditäre Faktoren eine relevante Rolle in der Pathogenese der Polyposis nasi spielen. Da eine familiäre Häufung, Alkohol- und Nikotinkonsum bislang in der Forschung nur unzureichend Beachtung fanden, sollte in prospektiven Studien ihre Auswirkung auf die Polypenbildung und insbesondere die Ergebnisse nach operativer Therapie ausführlich untersucht werden. Aufgrund unserer Ergebnisse wird die Hypothese aufgestellt, dass Alkoholkonsum und hereditäre Faktoren eine relevante Rolle in der Pathogenese der Polyposis nasi spielen. Da eine familiäre Häufung, Alkohol- und Nikotinkonsum bislang in der Forschung nur unzureichend Beachtung fanden, sollte in prospektiven Studien ihre Auswirkung auf die Polypenbildung und insbesondere die Ergebnisse nach operativer Therapie ausführlich untersucht werden. N2 - Englische Kurzfassung: In spite of intensive research in tue last decades, the ethiology and pathogenesis of chronic polypoid sinusitis remaines in the end widely unknown. Therefore a causal approach in the treatment is still missing, up to now the therapy of choice is the surgery of the affected nasal sinuses. However the high recurrence rates after surgical therapy show a big problem. A high association seems to be between the chronic polypoid sinusitis and accompanying illnesses like bronchial asthma ,aspirin intolerance and allergy. With the objective to detect which extent these influences have on the post surgical healing course and the recurrence rates, we observed in this study 54 patients who have been operated in the years 1991 up to and including 1993 in the university hospital for ear-, nose-, throat illnesses in Würzburg due to the primary diagnosis of nasal polyposis. The evaluation was done by the data from the patients files as well as by an especially developed questionnaire after a period of at least ten years post surgically. Beside the three accompanying illnesses the risk factors nicotine consumption and consumption of alcohol as well as the post surgical use of topical corticosteroids were correlated to tue datas of gender, age, post surgical symptoms, recurrence rates and the total number of operations per patient. In the examined patient's property the male gender was concerned predominantly, the patients were mostly at least thirty years old. Within ten years after surgery recurrence of nasal polyposis appeared in 22% of the patients. Approximately every 5-th patient with nasal polyposis (22%) suffered from bronchial asthma, 17% of the patients from aspirin intolerance. In our survey both illnesses showed no negative influence on the post surgical recurrence probability. About half of the patients were allergic subjekts, though recurrence of nasal polyposis in these persons occurs less frequently than in the non-allergic patients. This result supports the topical theses in the literature that allergies show no negative effect on chronic polypoid sinusitis. Our data to the post surgical local therapy with corticosteroids can confirm the information from the literature that topic given corticosteroids favour the healing of the nasal polyps and decrease recurrence rates. Because at a quarter of our patients the nasal polyps arose in at least one more family member, a genetic component can be supposed in the pathogenesis of the nasal polyposis. Among the fraction with the consumption of alcohol we clearly found higher recurrence rates than among the patients which denied this. In histologic works was already reported from a disturbance of the mucociliar clearance in the respiratory mucous membrane by alcohol. By this mechanism the use of alcohol could possibly favour the polyp growth. In our study nicotine had no influence on the polyp developement. On account of our results the hypothesis is put up that consumption of alcohol as well as hereditary factors play a major role in the pathogenesis of the chronic polypoid sinusitis. Because the cumulative familiar incidence of nasal polyps as well as the consumption of alcohol and nicotine found only insufficient attention up to now in the current literature, their effects should be examined in further prospective studies. KW - Nasennebenhöhlenentzündung KW - Bronchialasthma KW - Allergie KW - Rezidiv KW - Nasennebenhöhlenentzündung KW - Bronchialasthma KW - Allergie KW - Rezidiv KW - sinusitis KW - recurrence KW - asthma KW - allergy Y1 - 2008 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-27190 ER - TY - THES A1 - Hohaus, Andreas T1 - Intranasale versus intraperitoneale Applikation eines IL-4/IL-13-Antagonisten am murinen Asthmamodell T1 - Intranasal versus intraperitoneal application of an IL-4/IL-13-Antagonist in a mouse model for allergic asthma N2 - Asthma bronchiale ist eine chronische, entzündliche Erkrankung der Atemwege, charakterisiert durch bronchiale Hyperreaktivität und variable Atemwegs-obstruktion. Die Interleukine 4 und 13 sind entscheidend an den pathophysiologischen Vor-gängen beim allergischen Asthma bronchiale beteiligt. IL-4 gilt als spezifisches Zytokin für die Differenzierung von nativen T-Helferzellen zu TH2-Zellen. Gemeinsam mit IL-13 führt es zum Immunglobulinklassenswitch der B-Zellen. Ziel dieser Arbeit war es, in einem etablierten Mausmodell für allergisches Asthma verschiedene Applikationsformen des IL-4/IL-13-Antagonisten QY in ihrer Wirkung während der allergischen Sensibilisierung zu vergleichen. Dazu wurden Balb/c-Mäuse über einen Zeitraum von 6 Wochen wöchentlich mit 50µg OVA sensibilisiert. In zwei Therapiegruppen wurden zu jeder Sensibilisierung jeweils 10µg QY intranasal bzw. intraperitoneal verabreicht. Wöchentlich wurde das Serum der Versuchstiere auf allergenspezifische Antikörper untersucht. Nach sechs Wochen wurde eine bronchoalveoläre Lavage durchgeführt, um den Zytokingehalt und die allergeninduzierte Eosinophilie zu bestimmen. Sowohl die intranasale als auch die intraperitoneale Gabe von QY resultierte in einer signifikanten Abnahme allergenspezifischer IgE-Antikörper im Serum der Versuchstiere. Ebenso konnten die Zahl der inflammativen eosinophilen Granu-lozyten und der IL-5-Spiegel in der BAL signifikant gesenkt werden. Zusammenfassend wurde gezeigt, dass die prophylaktische Behandlung mit dem IL-4/IL-13-Antagonisten QY zuverlässig eine allergische Sensibilisierung der Versuchstiere verhindert. Die intranasale und intraperitoneale Applikation unterscheiden sich hierbei praktisch nicht in ihrer Wirksamkeit. N2 - IL-4 and IL-13 are considered as key regulators for the development of allergic asthma. This study compares intranasal versus intraperitoneal application of an IL-4/IL-13-Antagonist in a murine model for allergic asthma. In summary there is no significant difference between intranasal or intraperitoneal application. KW - Allergie KW - Asthma KW - Interleukin 4 KW - Interleukin 13 KW - Interleukinantagonist QY KW - allergy KW - asthma KW - interleukin 4 KW - interleukin 13 KW - interleukin antagonist Y1 - 2006 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-21533 ER - TY - JOUR A1 - Hohmann, Cynthia A1 - Pinart, Mariona A1 - Tischer, Christina A1 - Gehring, Ulrike A1 - Heinrich, Joachim A1 - Kull, Inger A1 - Melén, Eric A1 - Smit, Henriette A. A1 - Torrent, Maties A1 - Wijga, Alet H. A1 - Wickman, Magnus A1 - Bachert, Claus A1 - Lødrup Carlsen, Karin C. A1 - Carlsen, Kai-Håkon A1 - Bindslev-Jensen, Carsten A1 - Eller, Esben A1 - Esplugues, Ana A1 - Fantini, Maria Pia A1 - Annesi-Maesano, Isabella A1 - Momas, Isabelle A1 - Porta, Daniela A1 - Vassilaki, Maria A1 - Waiblinger, Dagmar A1 - Sunyer, Jordi A1 - Antó, Josep M. A1 - Bousquet, Jean A1 - Keil, Thomas T1 - The Development of the MeDALL Core Questionnaires for a Harmonized Follow-Up Assessment of Eleven European Birth Cohorts on Asthma and Allergies JF - International Archives of Allergy and Immunology N2 - Background: Numerous birth cohorts have been initiated in the world over the past 30 years using heterogeneous methods to assess the incidence, course and risk factors of asthma and allergies. The aim of the present work is to provide the stepwise proceedings of the development and current version of the harmonized MeDALL-Core Questionnaire (MeDALL-CQ) used prospectively in 11 European birth cohorts. Methods: The harmonization of questions was accomplished in 4 steps: (i) collection of variables from 14 birth cohorts, (ii) consensus on questionnaire items, (iii) translation and back-translation of the harmonized English MeDALL-CQ into 8 other languages and (iv) implementation of the harmonized follow-up. Results: Three harmonized MeDALL-CQs (2 for parents of children aged 4-9 and 14-18, 1 for adolescents aged 14-18) were developed and used for a harmonized follow-up assessment of 11 European birth cohorts on asthma and allergies with over 13,000 children. Conclusions: The harmonized MeDALL follow-up produced more comparable data across different cohorts and countries in Europe and will offer the possibility to verify results of former cohort analyses. Thus, MeDALL can become the starting point to stringently plan, conduct and support future common asthma and allergy research initiatives in Europe. KW - harmonization KW - MeDALL KW - european birth cohorts KW - asthma KW - allergy KW - questionnaire assessment Y1 - 2014 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-196594 SN - 1018-2438 SN - 1423-0097 VL - 163 IS - 3 ER - TY - THES A1 - Kneuer, Janine T1 - Therapie der obstruktiven Atemwegserkrankungen nach Stufenplan: Empfehlung und Realität T1 - Therapy of obstructive pulmonary disease according to the therapy plan: recommendation and reality N2 - Die vorliegende Studie beruht auf Daten von 254 Patienten, die im Zeitraum von 1990 bis 1998 stationär in die MedizinischeKlinik des Klinikums der Ludwig- Maximilians- UniversitätWürzburg eingewiesen worden sind. Die Patientengruppe bestand aus 120 Patienten mit der Entlassungsdiagnose Asthma und aus 134 Patienten mit der Entlassungsdiagnose COPD. Mittels Fragebögen wurden die Krankengeschichte sowie das aktuelle Krankheitsgeschehen erfaßt und statistisch ausgewertet. Das Hauptaugenmerk galt hierbei den verordneten Medikamenten. Als Basis diente der 1993 in einem Konsenspapier veröffentlichte Stufenplan der deutschen Atemwegsliga sowie der 1998 überarbeitete und auf die COPD Therapie erweiterte Stufenplan. In Bezug auf die Asthmatherapie stellte sich heraus, daß 55 % der Asthmapatienten zum Zeitpunkt ihrer stationären Aufnahme entsprechend des seit 1993 gültigen Stufenplanes behandelt worden sind. 32 % erhielten eine unzureichende und 10 % eine unsinnige bzw. unnötige Wirkstoffkombination. Mittels statistischer Methoden konnte eindeutig nachgewiesen werden, daß Patienten, die entsprechend des Stufenplanes behandelt worden sind, ein signifikant geringeres Risiko haben einen Status asthmaticus zu bekommen als Patienten ohne diese Therapie. Darüber hinaus hatten diese Patienten ein signifikant geringeres Rückfallrisiko. N2 - This study based on 254 in-patients, who were admitted between 1990 and 1998 into the Ludwig-Maximilian-University Hospital of Wuerzburg. This group was composed of 120 patients with the discharged diagnosis: asthma and 134 patients with the discharged diagnosis COPD. It was made an audit about the medical history and about the acute disease itself. This has been evaluated statistically. The main interest was aimed at the prescribed remedies compared with the therapy plan published in 1993 and revised in 1998 corresponding to the respective asthma stage. The result of this study was that 55% of the asthma patients were treated as demanded by the therapy plan of 1993. And 32% received an insufficient and 10% a useless medication. By means of statistical methods it was clearly proved that patients who were treate according to the therapy plan have a lower risk of being hit by a status asthmaticus than patients who were treated without this medication. And above all they have a lower recurrence risk. KW - Asthma KW - COPD KW - Stufenplan KW - Medikamente KW - asthma KW - COPD KW - therapy plan KW - drugs Y1 - 2002 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-5882 ER -