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IL-33 signalling contributes to pollutant-induced allergic airway inflammation.
Clin Exp Allergy 2018; 48(12):1665-1675CE

Abstract

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.

Authors+Show Affiliations

Department of Respiratory Medicine, Laboratory for Translational Research in Obstructive Pulmonary Diseases, Ghent University Hospital, Ghent, Belgium.Department of Respiratory Medicine, Laboratory for Translational Research in Obstructive Pulmonary Diseases, Ghent University Hospital, Ghent, Belgium.Center for Inflammation Research, Unit of Molecular Signal Transduction in Inflammation, VIB, Ghent, Belgium. Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.Department of Respiratory Medicine, Laboratory for Translational Research in Obstructive Pulmonary Diseases, Ghent University Hospital, Ghent, Belgium.Upper Airway Research Laboratory, Department of Otorhinolaryngology, Ghent University, Ghent, Belgium.Upper Airway Research Laboratory, Department of Otorhinolaryngology, Ghent University, Ghent, Belgium.Center for Inflammation Research, Unit of Molecular Signal Transduction in Inflammation, VIB, Ghent, Belgium. Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.Department of Respiratory Medicine, Laboratory for Translational Research in Obstructive Pulmonary Diseases, Ghent University Hospital, Ghent, Belgium.Department of Respiratory Medicine, Laboratory for Translational Research in Obstructive Pulmonary Diseases, Ghent University Hospital, Ghent, Belgium.Department of Respiratory Medicine, Laboratory for Translational Research in Obstructive Pulmonary Diseases, Ghent University Hospital, Ghent, Belgium.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

30159930

Citation

De Grove, Katrien C., et al. "IL-33 Signalling Contributes to Pollutant-induced Allergic Airway Inflammation." Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology, vol. 48, no. 12, 2018, pp. 1665-1675.
De Grove KC, Provoost S, Braun H, et al. IL-33 signalling contributes to pollutant-induced allergic airway inflammation. Clin Exp Allergy. 2018;48(12):1665-1675.
De Grove, K. C., Provoost, S., Braun, H., Blomme, E. E., Teufelberger, A. R., Krysko, O., ... Maes, T. (2018). IL-33 signalling contributes to pollutant-induced allergic airway inflammation. Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology, 48(12), pp. 1665-1675. doi:10.1111/cea.13261.
De Grove KC, et al. IL-33 Signalling Contributes to Pollutant-induced Allergic Airway Inflammation. Clin Exp Allergy. 2018;48(12):1665-1675. PubMed PMID: 30159930.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - IL-33 signalling contributes to pollutant-induced allergic airway inflammation. AU - De Grove,Katrien C, AU - Provoost,Sharen, AU - Braun,Harald, AU - Blomme,Evy E, AU - Teufelberger,Andrea R, AU - Krysko,Olga, AU - Beyaert,Rudi, AU - Brusselle,Guy G, AU - Joos,Guy F, AU - Maes,Tania, Y1 - 2018/09/19/ PY - 2018/01/25/received PY - 2018/07/27/revised PY - 2018/08/20/accepted PY - 2018/8/31/pubmed PY - 2019/11/15/medline PY - 2018/8/31/entrez KW - Air pollution KW - Airway epithelium KW - Asthma KW - Diesel Exhaust Particles KW - House Dust Mite KW - IL-33 and ST2 SP - 1665 EP - 1675 JF - Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology JO - Clin. Exp. Allergy VL - 48 IS - 12 N2 - 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. SN - 1365-2222 UR - https://www.unboundmedicine.com/medline/citation/30159930/IL_33_signalling_contributes_to_pollutant_induced_allergic_airway_inflammation_ L2 - https://doi.org/10.1111/cea.13261 DB - PRIME DP - Unbound Medicine ER -