IL ‐33 signalling contributes to pollutant‐induced allergic airway inflammation

Autor:	Katrien De Grove, Guy Joos, Harald Braun, Guy Brusselle, Olga Krysko, Tania Maes, Sharen Provoost, Rudi Beyaert, Andrea Renate Teufelberger, Evy E. Blomme
Rok vydání:	2018
Předmět:	0301 basic medicine Immunology Inflammation Respiratory Mucosa complex mixtures Mice 03 medical and health sciences 0302 clinical medicine Leukocytes Respiratory Hypersensitivity medicine Animals Immunology and Allergy Lymphocytes Asthma House dust mite Air Pollutants biology medicine.diagnostic_test Inhalation business.industry Pyroglyphidae Innate lymphoid cell Allergens respiratory system Interleukin-33 medicine.disease biology.organism_classification Interleukin-1 Receptor-Like 1 Protein Recombinant Proteins respiratory tract diseases Disease Models Animal 030104 developmental biology Bronchoalveolar lavage 030228 respiratory system Bronchial hyperresponsiveness Female Particulate Matter medicine.symptom Airway business Biomarkers Signal Transduction
Zdroj:	Clinical & Experimental Allergy. 48:1665-1675
ISSN:	1365-2222 0954-7894
DOI:	10.1111/cea.13261
Popis:	Background Clinical and experimental studies have identified a crucial role for IL-33 and its receptor ST2 in allergic asthma. Inhalation of traffic-related pollutants, such as diesel exhaust particles (DEP), facilitates the development of asthma and can cause exacerbations of asthma. However, it is unknown whether IL-33/ST2 signalling contributes to the enhancing effects of air pollutants on allergic airway responses. Objective We aim to investigate the functional role of IL-33/ST2 signalling in DEP-enhanced allergic airway responses, using an established murine model. Methods C57BL/6J mice were exposed to saline, DEP alone, house dust mite (HDM) alone or combined DEP+HDM. To inhibit IL-33 signalling, recombinant soluble ST2 (r-sST2) was given prophylactically (ie, during the whole experimental protocol) or therapeutically (ie, at the end of the experimental protocol). Airway hyperresponsiveness and the airway inflammatory responses were assessed in bronchoalveolar lavage fluid (BALF) and lung. Results Combined exposure to DEP+HDM increased IL-33 and ST2 expression in lung, elevated inflammatory responses and bronchial hyperresponsiveness compared to saline, sole DEP or sole HDM exposure. Prophylactic interference with the IL-33/ST2 signalling pathway impaired the DEP-enhanced allergic airway inflammation in the BALF, whereas effects on lung inflammation and airway hyperresponsiveness were minimal. Treatment with r-sST2 at the end of the experimental protocol did not modulate the DEP-enhanced allergic airway responses. Conclusion Our data suggest that the IL-33/ST2 pathway contributes to the onset of DEP-enhanced allergic airway inflammation.
Databáze:	OpenAIRE
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