Abstracts from the 11th Symposium on Experimental Rhinology and Immunology of the Nose (SERIN 2017)
2017; Springer Science+Business Media; Volume: 7; Issue: S3 Linguagem: Inglês
10.1186/s13601-017-0163-x
ISSN2045-7022
AutoresIbon Eguiluz Gracia, Carmen Rondón, Paloma Campo, Ana Prieto, Cristobalina Mayorga, Luisa Galindo, A. Criado Molina, Miguel Blanca, Marı́a José Torres, Taiyo Morikawa, Ayumi Fukuoka, Kazufumi Matsushita, Shigeharu Fujieda, Tomohiro Yoshimoto, Naruhito Iwasaki, Tamar Smulders, Danielle van Egmond, Kees van Drunen, Marc P. van der Schee, Achim Beule, Margot Berings, Anton Jult, Hanne Vermeulen, Natalie De Ruyck, Lara Derycke, Hakan Uçar, Philip Ghekiere, Robin Temmerman, John Ellis, Claus Bachert, Bart N. Lambrecht, Mélissa Dullaers, Philippe Gevaert, Stefania Arasi, Serena K. Perna, Yvonne Resch, Christian Lupinek, Kuan‐Wei Chen, Susanne Vrtala, Rudolf Valenta, Paolo Maria Matricardi, Ivânia Gonçalves, Tiago Jacinto, Rita Amaral, Ana Margarida Pereira, Luís Araújo, Mariana Couto, João Fonseca, Pär Stjärne, Ranbir Kaulsay, Wolfgang Pohl, Maria Carmen Plaza, Ana Maria Prieto, Cristobalina Mayorga, Magdalena Herknerová, Tengchin Wang, Chiejun Wu, Jonathan Kilimajer, Laura Pujols, Jordi Roca‐Ferrer, Francisco de Borja Callejas, Mireya Fuentes, María Pérez, Isam Alobid, Antonio Valero, César Picado, Ruth Murray, Joaquim Mullol, Brecht Steelant, Katleen Martens, Guy E. Boeckxstaens, Sven Seys, Peter W. Hellings, Timothy C. Biggs, Stephen M. Hayes, Philip G. Harries, Sylvia L. F. Pender, Rami J. Salib, Jean Kim, Hyun Sil Lee, Livije Kalogjera, Nada Vrkić, Anita Topić, Dejan Tomljenović, Tomislav Gregurić, P Radovanović, R. Jund, Pascal Haimerl, Adam Chaker, Yvonne Schober, Sonja Schindela, Andreas Nockher, Carsten B. Schmidt‐Weber, Julia Esser‐von Bieren, Pascal Ickrath, Norbert Kleinsasser, Niklas Beyersdorf, Xin Ding, Rudolf Hagen, Stephan Hackenberg, Daniela Cangiano, Francesco Cinetto, Giuseppe Brescia, Gino Marioni, Claudia Zanotti, Franco Schiavon, Roberto Padoan, Ilaria Caputo, Raffaella Neri, Carlo Agostini, Ji Heui Kim, Yong Ju Jang, Ji Youn Lim, Sung Hee Kim, Е. Л. Савлевич, Leonid Gaganov, Maria Kochnova, V.V. Egorov, Jie Shen Fok, Tanzeela Hanif, Jutta Renkonen, Sakari Joenväärä, Matti Kankainen, Mika J. Mäkelä, Paula Kauppi, Anna S. Pelkonen, Pirkko Mattila, Risto Renkonen, Sanna Toppila‐Salmi, Gabriële Holtappels, Bart N. Lambrecht, Natalia Blanca‐López, Miguel Gonzalez-Visiedo, Raquel Jurado‐Escobar, Gabriela Cantó,
Tópico(s)Asthma and respiratory diseases
ResumoOral Abstract Session 1: RhinitisO01 Long-term follow-up of local allergic rhinitis patientsIbon Eguiluz Gracia, Carmen Rondón, Paloma Campo, Ana Prieto, Lina Mayorga, Luisa Galindo, Ana Molina, Miguel Blanca, Maria Jose TorresHospital Regional Universitario de Malaga and IBIMA, Málaga, Spain Correspondence: Ibon Eguiluz Gracia - iboneguiluz@gmail.com Clinical and Translational Allergy 2017, 7(Suppl 3):O01 Introduction: There are few data available regarding natural history of local allergic rhinitis (LAR). We previously reported the results of the first 5-years of follow-up observing a similar rate of development of systemic allergic rhinitis (AR) in both LAR patients and healthy controls. Objective: To explore the natural history of a population with LAR and the development of AR and comorbidities over a 10 year period. Methods: A cohort of 194 patients with LAR of recent onset (<18 months) and 130 age- and sex-matched healthy controls were prospectively evaluated in a 10-year follow-up study (2005–2016). All participants provided informed consent and ethic committee of the hospital approved the study. Clinical-demographic questionnaire, spirometry, SPT and specific IgE (sIgE) to aeroallergens were evaluated yearly. Nasal allergen provocation tests (NAPT) with D. pteronyssinus (DP), Alternaria, Olea europea, and grass pollen were performed at baseline, and after 5 and 10 years. Results: A total of 151 patients (78%) and 90 controls (69%) completed the study. At baseline, most patients had moderate-to-severe persistent-perennial rhinitis. Conjunctivitis (52%) and asthma (19%) were the main comorbidities, and DP the most frequent sensitizing aeroallergen (51.1%). During the 10 years of evaluation 21 new cases of asthma (12.5%, P = 0.007) and 17 new cases of conjunctivitis (10%, P = 0.067) were diagnosed. After 10 years of evolution a similar rate of development of AR was detected in patients and healthy controls (11.3 vs 10%, P = 0.761). In 5 patients, conversion to systemic atopy occurred in the last year of evaluation (3%). Conclusions: LAR is a well-differentiated clinical entity with a low rate of development of systemic atopy. This study was funded by the Institute of Health “Carlos III” of the Spanish Ministry of Economy and Competitiveness through the RETICS ARADyAL (RD16/0006/0001) and the FIS PI14/00864. Keywords: Local allergic rhinitis, Allergic rhinitis, SensitizationO02 ILC2-activation aggravates Th2-dependent nasal inflammation in miceTaiyo Morikawa1, Ayumi Fukuoka1, Kazufumi Matsushita1, Shigeharu Fujieda2, Tomohiro Yoshimoto1 1Hyogo College of Medicine, Nishinomiya, Hyogo, Japan; 2University of Fukui, Fukui, Japan Correspondence: Taiyo Morikawa - taiyo1125@hotmail.co.jp Clinical and Translational Allergy 2017, 7(Suppl 3):O02 Introduction: It is well known that T helper (Th) 2 cells and group 2 innate lymphoid cells (ILC2s) contribute to allergic diseases. However, their exact role and relationship in nasal allergic disorders is unclear. We sought to investigate the cooperation of Th2 cells and ILC2s in a mouse model of nasal allergic disorder. Methods: To differentially activate Th2 cells and/or ILC2s in nasal mucosa, mice were intranasally administered ovalbumin (OVA) antigen, papain, an ILC2-activatior, or both for 2 weeks. Epithelial thickness and number of eosinophils in the nasal mucosa were evaluated at 24 h after the final challenge. Results: Intranasal administration of OVA and papain preferentially activated Th2 cells and ILC2s, respectively, in the nose. Both OVA and papain increased the nasal epithelial thickness and number of eosinophils, and their coadministration significantly enhanced the symptoms. ILC2- and Rag2-deficient mice showed a partial decrease in OVA-plus-papain-induced nasal epithelial thickening and eosinophilia. Interleukin (IL)-33- and ST2-deficient mice showed decreased OVA-plus-papain-induced, but not OVA-alone-induced nasal epithelial thickening and eosinophilia. IL-5 induced eosinophilia only, but IL-13 contributed to both nasal epithelial thickening and eosinophilia. Conclusions: IL-33/ST2-pathway-mediated ILC2 activation exacerbated additively Th2-cell-induced nasal type 2 inflammation. Furthermore, IL-13, but not IL-5, contributes to exacerbation of nasal type 2 inflammation. Keywords: Nasal allergy, Th2 cells, Group 2 innate lymphoid cells, IL-33, IL-13O03 Allergen endotoxins induce non-IgE-mediated nasal hypersensitivity in mice via monocyte/macrophage-dependent pathwayTomohiro Yoshimoto, Naruhito Iwasaki, Kazufumi MatsushitaHyogo College of Medicine, Nishinomiya, Japan Correspondence: Tomohiro Yoshimoto - tomo@hyo-med.ac.jp Clinical and Translational Allergy 2017, 7(Suppl 3):O03 Introduction: Allergen-mediated cross-linking of IgE on mast cells/basophils is a well-recognized trigger for type-1 allergic diseases such as allergic rhinitis (AR). However, allergens may not be the only trigger for AR, and several allergic-like reactions are induced by non-IgE-mediated mechanisms. Here, we describe a novel non-IgE-mediated, endotoxin-triggered nasal type-1-hypersensitivity reaction in mice. Methods: To investigate whether endotoxin affects sneezing responses, mice were intraperitoneally immunized with ovalbumin (OVA), and then nasally challenged with endotoxin-free or endotoxin-containing OVA. To investigate the role of T cells and mechanisms of the endotoxin-induced response, mice were adoptively transferred with in vitro differentiated OVA-specific Th2 cells, and then nasally challenged with endotoxin-free or endotoxin-containing OVA. Immediately after each nasal challenge, the frequency of sneezing was counted for 10 min. The mice were sacrificed 24 h after the final nasal challenge, and noses were dissected for analyzing infiltrating inflammatory cells. Results: Endotoxin-containing, but not endotoxin-free, OVA elicited sneezing responses in mice independent from IgE-mediated signaling. OVA-specific Th2 cell adoptive transfer to mice demonstrated that local activation of antigen-specific Th2 cells was required for the response. The Toll-like receptor 4-MyD 88-signaling pathway was indispensable for endotoxin-containing OVA-elicited rhinitis. In addition, lipopolysaccharide directly triggered sneezing responses in OVA-specific Th2-transferred and nasally endotoxin-free OVA-primed mice. Although an antihistamine, diphenhydramine, suppressed sneezing responses, mast-cell/basophil-depleted mice had normal sneezing responses to endotoxin-containing OVA. Clodronate treatment abrogated endotoxin-containing OVA-elicited rhinitis, suggesting the involvement of monocytes/macrophages in this response. Conclusions: Antigen-specific nasal activation of CD4+ T cells followed by endotoxin exposure induces mast cell/basophil-independent histamine release in the nose that elicits sneezing responses. Thus, environmental or nasal residential bacteria may exacerbate AR symptoms. In addition, this novel phenomenon might explain currently unknown mechanisms in non–IgE-mediated allergic disorders, such as non-IgE-mediated gastrointestinal food allergy in infants. Keywords: Non-allergic rhinitis, Endotoxin, Histamine, T cells, Monocytes/macrophages
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