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IL ‐33 signalling contributes to pollutant‐induced allergic airway inflammation
Author(s) -
De Grove Katrien C.,
Provoost Sharen,
Braun Harald,
Blomme Evy E.,
Teufelberger Andrea R.,
Krysko Olga,
Beyaert Rudi,
Brusselle Guy G.,
Joos Guy F.,
Maes Tania
Publication year - 2018
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/cea.13261
Subject(s) - inflammation , immunology , signalling , airway , allergic inflammation , medicine , biology , microbiology and biotechnology , surgery
Summary Background Clinical and experimental studies have identified a crucial role for IL ‐33 and its receptor ST 2 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/ ST 2 signalling contributes to the enhancing effects of air pollutants on allergic airway responses. Objective We aim to investigate the functional role of IL ‐33/ ST 2 signalling in DEP ‐enhanced allergic airway responses, using an established murine model. Methods C57 BL /6J mice were exposed to saline, DEP alone, house dust mite ( HDM ) alone or combined DEP + HDM . To inhibit IL ‐33 signalling, recombinant soluble ST 2 (r‐ sST 2) 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 ST 2 expression in lung, elevated inflammatory responses and bronchial hyperresponsiveness compared to saline, sole DEP or sole HDM exposure. Prophylactic interference with the IL ‐33/ ST 2 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‐ sST 2 at the end of the experimental protocol did not modulate the DEP ‐enhanced allergic airway responses. Conclusion Our data suggest that the IL ‐33/ ST 2 pathway contributes to the onset of DEP ‐enhanced allergic airway inflammation.