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The role of mast cells, interleukin-13 and transient receptor potential channels in a mouse model of chemical-induced airway hyperresponsiveness


Occupational asthma is the most common work-related lung disease in industrialized countries. The mechanisms of occupational asthma caused by chemicals are still not completely understood. Therefore, we used a mouse model of chemical-induced asthma to examine the role of the neurogenic system as well as the role of IL-13 and mast cells by using different knock-out mice.


On days 1 and 8, wild type C57Bl/6 mice, IL-13, TRP (Transient Receptor Potential) A1, TRPV1 and mast cell deficient mice were dermally sensitized with 1% TDI (toluene-2.4-diisocyanate) or vehicle (acetone/olive oil) on both ears. On day 15, the mice received a single intranasal challenge with 0.1% TDI or vehicle. In a second experiment TDI or vehicle sensitized wild type C57Bl/6 mice received an intraperitoneal injection of the NK1R antagonist RP67580 (1µg/µl) prior to the challenge. Airway reactivity to methacholine, lung inflammation, lymphocyte subpopulations in the draining auricular lymph nodes and total serum IgE were assessed 24h after the challenge.


IL-13, TRPV1, TRPA1 and mast cell deficient mice showed a significant lower airway hyperreactivity compared to wild type mice, 24h after TDI challenge, without any sign of lung inflammation. Treatment with the NK1R antagonist also resulted in a significant decrease in airway hyperreactivity. In the auricular lymph nodes T-helper cells, T-cytotoxic cells and B-cells were significantly lower in mast cell deficient and IL-13 deficient mice, compared to wild type mice.


These results indicate the importance of IL-13, TRPA1 and TRPV1 channels and mast cells in the development of immune-mediated bronchial hyperreactivity.

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This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Devos, F., De Vooght, V., Nemery, B. et al. The role of mast cells, interleukin-13 and transient receptor potential channels in a mouse model of chemical-induced airway hyperresponsiveness. Clin Transl Allergy 3 (Suppl 2), P31 (2013).

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