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Clinical and Translational Allergy

Open Access

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

  • Fien Devos1,
  • Vanessa De Vooght1,
  • Benoit Nemery1,
  • Peter Hoet1 and
  • Jeroen Vanoirbeek1
Clinical and Translational Allergy20133(Suppl 2):P31

https://doi.org/10.1186/2045-7022-3-S2-P31

Published: 16 July 2013

Background

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.

Method

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.

Results

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.

Conclusion

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

Authors’ Affiliations

(1)
KU Leuven, Occupational, Environmental and Insurance Medicine, Leuven, Belgium

Copyright

© Devos et al; licensee BioMed Central Ltd. 2013

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 (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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